Akio Tateishi

Feasibility of the Titration Method of Mild Hypothermia in Severely Head-injured Patients with Intracranial Hypertension

OBJECTIVE Clinical strategy to maximize effectiveness and to minimize adverse influences remains to be determined for mild hypothermia therapy for traumatic brain injury. This study was conducted to evaluate the clinical feasibility of the titration method of mild hypothermia in severely head-injured patients in whom a reduction in intracranial pressure was regarded as the target effect. METHODS Nine consecutive patients with severe head injury were studied. Patient age ranged between 18 and 66 years, Glasgow Coma Scale scores were equal to or less than 8, and intracranial pressures were equal to or greater than 20 mm Hg despite removal of intracranial hematoma and drugs, including glycerol and thiopental. During a maximum of 6 days of hypothermia therapy, jugular venous blood or cerebrospinal fluid temperature was titrated to reduce intracranial pressure to less than 20 mm Hg by means of repeated intragastric cooling with our nasoduodenal tube and surface cooling. The feasibility and the effects on systemic complications of this titration method of mild hypothermia were evaluated. RESULTS Intracranial pressure variably decreased from before to 3 hours after the beginning of all procedures of cooling. The mean intracranial pressure significantly decreased from 24 to 15 mm Hg with cooling, while temperature reduced an average of 2.0 degrees C. Four patients had systemic infection complications. Increased C-reactive protein and decreased platelet count were observed in all patients during hypothermia. The incidence of good recovery and moderate disability according to the Glasgow Outcome Scale was seven of nine patients. CONCLUSION The titration method of mild hypothermia to control intracranial hypertension in severely head-injured patients is clinically feasible. However, the method failed to reduce the incidence of infectious and hematological complications.

Qualitative comparison of carbon dioxide-induced change in cerebral near-infrared spectroscopy versus jugular venous oxygen saturation in adults with acute brain disease

OBJECTIVE To compare carbon dioxide-induced changes in cerebral oxy- and deoxyhemoglobin, measured by near-infrared spectroscopy, with those changes in jugular venous oxygen saturation in adult patients with acute brain disease. DESIGN A prospective study. SETTING The medical and surgical intensive care unit of a university hospital. PATIENTS Nine patients with head trauma (n = 4), cerebrovascular disease (n = 3), and meningitis (n = 2). A total of ten measurements were done, while PaCO2 was increased from hypocapnia toward normocapnia in the nine patients. INTERVENTIONS Arterial and jugular bulb catheterization, and intracranial pressure monitoring were performed as a part of the clinical intervention. An increase in PaCO2 was obtained by inhalation of CO2 and, if necessary, by reducing the ventilator rate. MEASUREMENTS AND MAIN RESULTS In each patient, the position of the jugular bulb catheter was ascertained by skull roentgenography. Near-infrared spectroscopic values for oxy- and deoxyhemoglobin were set at zero at the beginning of the study. An increase in PaCO2 from 29 +/- 1 (SEM) torr (3.9 +/- 0.2 kPa) to 39 +/- 2 torr (5.2 +/- 0.3 kPa) was accompanied by a significant increase in jugular venous oxygen saturation from 63 +/- 3% to 76 +/- 3%; a significant increase in oxyhemoglobin of 3.5 +/- 0.9 mumol/L (of the brain tissue); and a significant decrease in deoxyhemoglobin of 1.5 +/- 0.4 mumol/L. In nine of ten measurements, the slopes of changes in oxyhemoglobin against the slopes of change in jugular venous oxygen saturation were very similar. In one patient, oxyhemoglobin changed negligibly while jugular venous oxygen saturation increased by 20%. CONCLUSIONS Jugular venous oxygen saturation consistently demonstrates cerebrovascular responsiveness to CO2. The direction and magnitude of changes in cerebral oxyhemoglobin, measured by near-infrared spectroscopy, were similar to those changes in jugular venous oxygen saturation in most of our cases. Interpretation of a negligible change in oxyhemoglobin in one patient, despite an obvious increase in jugular venous oxygen saturation, requires further study comparing near-infrared spectroscopy with standard techniques.

Intracranial pressure following cardiopulmonary resuscitation

Intracranial pressure (ICP) was measured in six patients following cardiopulmonary resuscitation (CPR). The causes of cardiac arrest were respiratory or circulatory problems and the primary intracranial pathology was not detected. The measurement of ICP started 3 to 10 h following CPR except one patient in whom it started on the day 7. Duration of ICP measurement ranged from 2 to 7 days. In five out of six patients, ICP persistently remained below 20 mmHg. In the remaining one patient, ICP elevation associated with seizure activity was observed and ICP ultimately increased to 57 mmHg. Among these, four patients died and two remained in a persistent vegetative state. These results suggest that ICP following CPR does not necessarily increase if the patient has no primary intracranial pathology or seizures.

Nicardipine increases cerebral blood flow but does not improve neurologic recovery in a canine model of complete cerebral ischemia

The effects of the calcium entry blocker nicardipine on CBF, CMRO2, and neurologic outcome following 10 min of complete cerebral ischemia were examined in dogs. In CBF and CMRO2 studies, the CBF in the untreated group (seven dogs) and the nicardipine group (seven dogs; 20 μg kg−1 at 30 min postischemia and a subsequent infusion of 2 μg kg−1 min−1 for 90 min) initially increased to 300–400% and then returned to preischemic values at 30 min postischemia. Thereafter the CBF in the untreated group significantly decreased to 50% of preischemic values for the following 90-min period (hypoperfusion), while the CBF in the nicardipine group did not differ from preischemic values. The CMRO2 in both groups decreased to ∼50–80% of preischemic values after 15 min postischemia and did not differ between the groups throughout the study. In neurologic outcome studies, 18 dogs were divided into three groups (of six dogs each): untreated; saline infusion only, posttreated; nicardipine as in CBF and CMRO2 studies, pretreated; nicardipine 20 μg kg−1 at 2 min preischemia and a subsequent infusion of 2 μg kg−1 min−1 from immediately postischemia to 120 min postischemia. Nicardipine treatment initiated either before or after ischemia failed to improve neurologic outcome at 48 h postischemia. Thus, the increase of postischemic global CBF by nicardipine is not accompanied by neurologic recovery in a canine model of complete cerebral ischemia.

Cerebral Circulation and Metabolism during Enflurane Anesthesia in Humans

The effects of enflurane anesthesia on cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRo2) were studied in 17 patients. The patients were divided into two groups according to the depth of anesthesia. Cerebral perfusion pressure was maintained above 60 mmHg with phenylephrine. In Group 1 (arterial enflurane concentration, 15 mg/dl), patients were studied before surgery, while in group 2 (enflurane concentration, 27 mg/dl), the measurements were performed before and during surgery. In Group 1, mean CBF and CMRo2 were 53 and 2.8 ml · 100 g-1 · min-1, respectively. These values were not significantly different from CBF (46 ml · 100 g-1 · min-1) and CMRo2 (3.1 ml · 100 g-1 · min-1) values previously obtained in awake patients. In Group 2 before surgery, mean CBF and CMRo2 were 61 and 2.6 ml · 100 g-1 · min-1, respectively, and were significantly different from the awake values, while the EEG showed frequent spikes and suppression. In Group 2 during surgery, mean CBF and CMRo2 did not differ from the values obtained before surgery, despite significant EEG changes. The results indicate that enflurane is a cerebral vasodilator and causes an increase in CBF and a decrease in CMRo2 in humans at an anesthetic level characterized by frequent spikes and suppression on the EEG.

HBV-related fulminant hepatic failure: successful intensive medical therapy in a candidate for liver transplantation

Fulminant hepatic failure (FHF) usually has a fatal prognosis without liver transplantation. We describe the case of a woman who developed FHF, and was evaluated as a candidate for liver transplantation, but who was cured without transplantation through intensive medical care that included glucagon-insulin therapy, methylprednisolone pulse therapy, interferon beta and lamivudine administration, cyclosporine administration, and high-volume hemodiafiltration and plasma exchange. In a patient with FHF who is a candidate for liver transplantation but for whom the transplantation cannot be performed for some reason, intensive medical therapy, including regeneration-promoting therapy, immunosuppressive therapy, antiviral therapy, and vigorous hepatic support, should be carried out.

Long-Term Heart Rate Fluctuations in Postoperative and Brain-Dead Patients

Long-term heart rate fluctuations in postoperative and brain-dead patients were investigated. Heart rates were monitored continuously, and the data were stored, edited, and interpolated to allow for data lost during calibration and disconnection of the sensors for various treatments. Heart rate power spectra were calculated using the fast Fourier transform method. The power spectra of the patients who recovered showed that the heart rate fluctuated and produced a 1/f relationship, termed 1/f fluctuations, whereas those of patients who died in the intensive care unit (ICU) consisted of white-noise-like signals. The power spectra in brain-dead patients showed a 1/f relationship under steady-state conditions, while the power density and variation of the frequency distribution were lower than those in a normal subject. Therefore, 1/f fluctuations appear to be universal and occur independent of the central nervous system.

Cardiac arrest after traffic accident induced through vagal reflex in a case with bilateral stenosis of vertebral arteries

An 84-year-old driver suffered cardiac arrest after a traffic accident. He was quickly resuscitated and transferred to a hospital where he was treated in a state of unconsciousness and respiratory failure for 20 days until his death. The brain stem was rendered anoxic during cardiac arrest, which caused the respiratory failure. Artificial ventilation and catecholamine infusion were carried out, resulting in myocardial degeneration. Bilateral stenosis of the vertebral arteries was disclosed, but no injuries or hemorrhage of the brain and spinal cord were detected. On days 3 and 4 after admission, immediately after the head of the victim was flexed forward for examinations, cardiac arrest was induced twice, but was controlled either by administering atropine or by restoring the original posture. Positional change is known to induce vagal reflex that results in bradycardia, hypotension or cardiac arrest in sensitive persons. The victim might have undergone the reflex-mediated cardiac arrest after the accident, to which the stenosis of the vertebral arteries may have contributed.

Mild Hypothermia Therapy for Severe Acute Brain Insults in Clinical Practice

Animal experiments have provided persuasive evidence that mild hypothermia confers significant protection against ischemic or traumatic brain insults. Therefore, it is very important to establish a safe and secure procedure for mild hypothermia therapy in clinical practice.

Heart rate fluctuations in post‐operative and brain‐death patients

The power spectra of heart rate in patients receiving intensive care were calculated and the relation between gain and frequency discussed. 1/f fluctuations in heart rate can be observed in both post‐operative and brain‐death patients in the intensive care unit. These results suggested that 1/f fluctuations are a fundamental human phenomenon.