Takashi Tokutomi

Optimal temperature for the management of severe traumatic brain injury: effect of hypothermia on intracranial pressure, systemic and intracranial hemodynamics, and metabolism.

OBJECTIVEWe studied the effect of hypothermia on intracranial pressure, systemic and intracranial hemodynamics, and metabolism in patients with severe traumatic brain injury to clarify the optimal temperature for hypothermia, with a view toward establishing the proper management techniques for such patients. METHODSThe study was performed in 31 patients with severe head injury (Glasgow Coma Scale score as high as 5). All patients were sedated, paralyzed, ventilated, and cooled to 33°C. Brain temperature, core temperature, intracranial pressure, cerebral perfusion pressure, jugular venous oxygen saturation, mixed venous oxygen saturation, cardiac output, oxygen delivery, oxygen consumption, and resting energy expenditure were monitored continuously. RESULTSIntracranial pressure decreased significantly at brain temperatures below 37°C and decreased more sharply at temperatures 35 to 36°C, but no differences were observed at temperatures below 35°C. Cerebral perfusion pressure peaked at 35.0 to 35.9°C and decreased with further decreases in temperature. Jugular venous oxygen saturation and mixed venous oxygen saturation remained in the normal range during hypothermia. Resting energy expenditure and cardiac output decreased progressively with hypothermia. Oxygen delivery and oxygen consumption decreased to abnormally low levels at rectal temperatures below 35°C, and the correlation between them became less significant at less than 35°C than that when temperatures were 35°C or higher. Brain temperature was consistently higher than rectal temperature by 0.5 ± 0.3°C. CONCLUSIONThese results suggest that, after traumatic brain injury, decreasing body temperature to 35 to 35.5°C can reduce intracranial hypertension while maintaining sufficient cerebral perfusion pressure without cardiac dysfunction or oxygen debt. Thus, 35 to 35.5°C seems to be the optimal temperature at which to treat patients with severe traumatic brain injury.

Effect of 35°C Hypothermia on Intracranial Pressure and Clinical Outcome in Patients With Severe Traumatic Brain Injury

BACKGROUND From 1994, we have used therapeutic hypothermia in patients with severe traumatic brain injury (Glasgow Coma Scale scores of 5 or less). In 2000, we altered the target temperature to 35 degrees C from the former 33 degrees C, as our findings suggested that cooling to 35 degrees C is sufficient to control intracranial hypertension, and that hypothermia below 35 degrees C may predispose patients to persistent cumulative oxygen debt. We attempted to clarify whether 35 degrees C hypothermia has the same effect as 33 degrees C hypothermia in reducing intracranial hypertension and whether it is associated with fewer complications and improved outcomes. METHODS We compared intracranial pressure (ICP) and biochemical parameters in the 30 patients treated with 35 degrees C hypothermia (January 2000 to June 2005) with those in the 31 patients treated with 33 degrees C hypothermia (July 1994 to December 1999). RESULTS Patient characteristics were similar in the two groups. The mean temperature during hypothermia was 35.1 +/- 0.7 degrees C in the 35 degrees C hypothermia group and 33.4 +/- 0.8 degrees C in the 33 degrees C hypothermia group. Mean ICP was controlled under 20 mm Hg during hypothermia in both the 35 degrees C hypothermia and 33 degrees C hypothermia groups. The incidence of intracranial hypertension and low cerebral perfusion pressure did not differ between the two groups. The 35 degrees C hypothermic patients exhibited a significant improvement in the decline of serum potassium concentrations during hypothermia and in the increment of C-reactive protein after rewarming. The mortality rate and the incidence of systemic complications tended to be lower in the 35 degrees C group. CONCLUSIONS Cooling patients to 35 degrees C is safe and the ICP reduction effects of 35 degrees C hypothermia are similar to those of 33 degrees C hypothermia.

Age-Associated Increases in Poor Outcomes after Traumatic Brain Injury: A Report from the Japan Neurotrauma Data Bank

Age is an important factor influencing outcome after severe traumatic brain injury (TBI). In general, the older the victim, the higher the probability of a poor outcome. To investigate the mechanism underlying the link between age and outcome, the data for 797 patients enrolled in the Japan Neurotrauma Data Bank (JNTDB), aged 6 years or older, with Glasgow Coma Scale (GCS) scores of 8 or less on admission or deterioration to that level within 48 h of impact were analyzed. Thirty-eight percent of the patients were between the ages of 40 and 69 years, and 24% of the patients were older than 69 years. Older patients had higher rates of mortality and lower rates of favorable outcome. The frequency of mass lesions which were associated with poorer outcomes significantly increased with age, but regardless of the intracranial lesion type, older patients had poorer outcomes. The GCS score and the occurrence of systemic complications did not differ significantly according to age. Multiple systemic injury was less frequent in older patients. The varied occurrence of intracranial lesion types according to age is likely caused by the disparity between the young and aged brain in the progression of secondary brain injury. Alteration in the pathophysiological response, which is related to the development of secondary brain injury in the aging brain, probably contributes to more severe and irreversible brain damage in older patients, and is thus associated with poor outcomes.

Effect of hypothermia on serum electrolyte, inflammation, coagulation, and nutritional parameters in patients with severe traumatic brain injury.

Introduction: We evaluated the effect of induced hypothermia on biochemical parameters in patients with severe traumatic brain injury.Methods: We obtained hemoglobin, hematocrit, white blood count, lymphocyte count, platelet count, and serum concentrations of sodium, potassium, glucose, albumin, and C-reactive protein, and prothrombin time, hepaplastin test, activated partial thromboplastin time, antithrombin-III, α2PI, and nitrogen excretion on the day of admission, and on days 1, 3, 5, 7, 14, and 21 after the injury in 31 patients with severe head injury who were treated with hypothermia of 33°ranging from 48 to 72 hours. We selected 33 normothermic patients as a control group; these patients were selected from patients who had been treated before hypothermia was used as a treatment modality, by the same criteria for hypothermia therapy. We compared the biochemical markers and rectal temperature and intracranial pressure in the hypothermia group with those in the normothermia group. Outcome was assessed using the Glasgow Outcome Scale at 6 months after injury.Results: The demographic characteristics, severity, and outcome were similar in the hypothermia and normothermia group. Intracranial pressure was significantly decreased by hypothermia. Serum potassium concentration decreased significantly during hypothermia. White blood cell counts and C-reactive protein levels were higher after rewarming in the hypothermia group, and these were also higher in the patients with infectious complications, although the incidence of infectious complications did not differ between the hypothermia and normothermia groups. There were no statistically significant prolongations of activated partial thromboplastin time and no decline in prothrombin time with hypothermia. Platelet count, antithrombin-III, and α2PI did not differ significantly between the two groups.Conclusion: Hypothermia of 33° for 48–72 hours does not appear to increase the risk for coagulopathy and infections, although hypothermic patients exhibited significant increments in inflammatory markers such as C-reactive protein and white blood counts after rewarming.

Neurochemical monitoring in the management of severe head-injured patients with hypothermia

Abstract The neuroprotective action and effect of hypothermia on the neurochemical system is not well understood. The present study was performed using six patients with GCS scores of 5 or less to clarify the relationship between monitored brain temperature, intracranial pressure (ICP), cerebral perfusion pressure (CPP) and oxygen saturation of the jugular venous blood (SjO2). Changes in concentration of excitatory amino acids, glutamate (CLU) and aspartate (ASP), and NO2 were studied using intracerebral microdialysis as well as in jugular venous blood and cerebrospinal fluid (CSF). Changes in brain temperature, CPP and SjO2 resulting from hypothermia and brain death associated with markedly higher concentrations of and fluctuations in the concentrations of CLU, ASP and NO2 were observed in the dfalysate than in the jugular venous blood or CSF. Hypothermic treatment significantly reduces excitatory amino acid and NO2 concentrations, a finding which was associated with an improvement in CPP and SjO2. Measurement of CLU and ASP using intracerebral microdialysis is a clinically useful method for clarifying abnormal neurochemical events associated with severe head injury and for evaluating the effects of hypothermia. [Neurol Res 2000; 22: 657-664]

Cranioplasty with split lateral skull plate segments for reconstruction of skull defects.

This paper reports the use of cranioplasty using segments of split lateral skull plate to correct large skull defects (larger than 8 x 8 cm). The subjects consisted of 10 patients with head trauma who had undergone decompression surgery, and two patients who had undergone tumour resection. Bone grafts were obtained by cutting approximately 2 cm wide strips from the lateral skull plate using a bone saw that was inserted from a free margin of the bone defects. By cutting strips laterally from the bone defect, the necessary amount of split lateral skull plate can be obtained without performing craniotomy. The pieces of split lateral skull plate are then fixed to the defect using wire or titanium mini-plates. At this point, the selection of bone grafts that match the curvature of the dura mater is important, so that no dead spaces are created between the dura mater and the bone grafts. Infection was not detected in any of the 12 patients, and all bone grafts took completely. One of the 12 patients suffered from a pathological fracture and bone resorption 6 months after surgery. The fracture occurred because the use of basket-shaped reconstruction plates resulted in large spaces between the plate segments, and in addition the intracranial pressure was kept low by a V-P shunt, thus rendering the patient more vulnerable to atmospheric pressure.

Intracranial haemodynamics in diffuse and focal brain injuries. Evaluation with transcranial Doppler (TCD) ultrasound

SummaryIntracranial haemodynamics were studied in 20 patients with diffuse and focal brain injury and experimental animals with acute intracranial hypertension by the use of TCD ultrasound. The mean flow velocity in the middle cerebral artery (MCA) commonly decreased on the side of the haematoma depending on intracranial pressure (ICP) elevation and cerebral perfusion pressure (CPP) reduction in focal injury. The decrease of the MCA flow velocity returned to normal after treatment. The flow velocities decreased bilaterally and there was no difference between the right and left side in diffuse injury. But the velocities increased in spite of ICP elevation when diffuse cerebral swelling developed. Cerebrovascular CO2 reactivity was impaired in two groups of patients with low Glasgow Coma Scale (GCS) scores. The mean velocity of the MCA and blood flow in the internal carotid artery exhibited flow patterns which changed correlatively depending on CPP reduction in experimental animals. Noninvasive study by use of TCD ultrasound can provide valuable information on variant haemodynamic phenomena in patients with diffuse and focal brain injury.

Intraventricular Malignant Triton Tumour

Summary¶ The authors present the clinical and pathological features of a malignant triton tumour (MTT) in the lateral ventricle with neurofibromatosis type 1. A 57 year-old man presented with disorientation and memory disturbance. A Computed tomographic scan and magnetic resonance imaging studies revealed an enhancing lesion in the left lateral ventricle. A parieto-occipital transcallosal approach was taken and resection of the lesion was performed. The operative findings suggested that the tumour arose from the perivascular nerves. The final pathological diagnosis was a MTT. This is the first case of an intraventricular MTT. Aggressive treatment including radical surgery combined with radiochemotherapy is recommended for a MTT of the central nervous system.

Monitoring of Severe Head-Injured Patients with Transcranial Doppler (TCD) Ultrasonography

Intracranial haemodynamics were studied in 36 patients with severe head injury and experimental animals with acute intracranial hypertension by the use of TCD ultrasound. The mean flow velocity (FV) in the basal cerebral arteries commonly decreased on the side of the haematoma depending on intracranial pressure (ICP) elevation and cerebral perfusion pressure (CPP) reduction in focal brain injury. The FV decreased bilaterally and there was no difference between the right and left sides in diffuse brain injury without a clear relationship between the FV and CPP. The FV of the middle cerebral artery and blood flow in the internal carotid artery exhibited flow patterns which changed correlatively depending on CPP reduction in experimental animals. Monitoring with TCD ultrasound is valuable in evaluating compression ischaemia in focal brain injury. But many complicated factors are considerable in diffuse brain injury.

Syringobulbia Caused by Delayed Postoperative Tethering of the Cervical Spinal Cord – Delayed Complication of Foramen Magnum Decompression for Chiari Malformation

Summary Postoperative tethering of the high cervical spinal cord is a rare cause of neurological deterioration after foramen magnum decompression (FMD) with duraplasty for Chiari type I malformation. A review of the literature revealed that only 5 cases have been reported. This entity is not widely known to occur as a complication of the common surgical procedure for Chiari type I malformation. A 17-year-old boy experienced rapidly progressive neurological deterioration over a 3-month period. FMD and duraplasty with lyophilized cadaver dura had been performed 8 years previously. Follow-up MR images showed that the cerebrospinal fluid (CSF) space dorsal to the cord was gradually disappearing and that syringobulbia had developed. Opening the dura mater of the posterior fossa revealed dense fibrous scarring, arachnoid thickening over the cervicomedullary area, and tethering the cord to the dura from the medulla to C2. The adhesions were dissected free, and the tethering was released. A syringosubarachnoid (SS) shunt was inserted and duraplasty was performed with an expended polytetrafluoroethylene sheet (Gore-Tex). Postoperative MR images demonstrated that the syringobulbia had completely collapsed and that a dorsal CSF space was present. Follow-up MR images provided significant information on the cervical spinal cord tethering after FMD with duraplasty for Chiari malformation. We encourage sharp surgical detethering and duraplasty with Gore-Tex to avoid retethering. Early recognition and treatment of this unusual but important complication are emphasized.