A case of cervical pneumorrhachis induced by the combination of pneumomediastinum and root avulsion injuries.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Akira Takasu.
Explore the source record for details and available documents.
PURPOSE: To identify candidates indicated to undergo induced hypothermic therapy (IHT) among comatose survivors of out-of-hospital cardiopulmonary arrest (CPA) based on a retrospective review of medical charts. METHODS: Between 1995 and 2004, 49 patients who recovered from CPA and treated by IHT were analyzed. The subjects were divided into 2 groups. The first group (GR, n = 16) consisted of patients with a recovery of consciousness and the second group (VD, n = 33) consisted of patients who either remained unconscious or who died. RESULTS: Using a multiple logistic regression analysis, out-of-hospital return of spontaneous circulation was the only factor independently associated with the outcome (odds ratio, 0.03; 95% confidence interval, 0.00-0.23; P = .001). CONCLUSION: IHT may be beneficial for CPA patients with out-of-hospital return of spontaneous circulation. Because of the small sample size, further large human studies are warranted.
BACKGROUND: Rapid induction of hypothermia has been shown to improve survival in uncontrolled hemorrhagic shock (UHS) rat studies. We hypothesized that prolonged induction of hypothermia would be equally beneficial for survival during UHS. METHODS: Light anesthesia was induced with halothane in 30 rats, and spontaneous breathing was maintained. Rectal temperature (Tr) was monitored and maintained at 38 degrees C. UHS was induced by blood withdrawal of 2.5 mL/100 g during a 15-minute period, followed by 75% tail amputation. Immediately after cutting the tail, rats were randomized into three groups of 10 rats each: Group 1, maintained at Tr 38 degrees C; group 2, passively cooled to 34 degrees C by exposure to room temperature (23 degrees C); and group 3, actively cooled to 34 degrees C by applying alcohol to the skin and under an electric fan. Next, rats were controlled at each target Tr and observed without fluid resuscitation until either death or a maximum of 240 minutes. RESULTS: Cooling rate was -0.09 +/- 0.01 degrees C/min in group 2 and -0.36 +/- 0.9 degrees C/min in group 3 (p < 0.01). Mean survival time was 72 +/- 21 minutes in group 1 (38 degrees C), and was nearly doubled by hypothermia to 132 +/- 62 minutes for group 2 (p < 0.01 vs. group 1) and 150 +/- 69 minutes for group 3 (p < 0.01 vs. group 1). No significant difference in survival was noted between groups 2 and 3. Additional blood loss from the tail stump did not differ significantly between groups. CONCLUSION: Therapeutic mild hypothermia, induced either slowly (approximately -0.1 degrees C/min) or rapidly (approximately -0.4 degrees C/min) prolongs survival during lethal UHS in rats.
Explore the source record for details and available documents.
OBJECTIVE: Controlled hypothermia induced during hemorrhagic shock (HS) has been shown previously to improve survival in HS rat outcome models. We hypothesized that hypothermia (34 degrees C) induced immediately with reperfusion would also improve survival. METHODS: Twenty-four rats were lightly anesthetized with halothane and maintained spontaneous breathing. The rats underwent: an HS phase I of 75 min, with an initial blood withdrawal of 2.5 mL/100 g over 15 min, followed by either additional blood withdrawal or re-infusion in order to maintain a mean arterial pressure (MAP) of 30 mmHg over 60 min; a resuscitation phase II of 60 min with return of shed blood and infusion of lactated Ringer's solution to maintain a MAP of 75 mmHg; and an observation phase III without anesthesia for 72 h. Five minutes before the start of phase II, 12 rats were randomized into either a normothermia (38 degrees C) group or hypothermia (34 degrees C) group. The rectal temperature in each group was carefully maintained during the 60-min period of phase II. Survival at 72 h, as well as gut damage were assessed. RESULTS: All 24 rats survived beyond phases I and II. At 72 h, 8 of 12 rats survived in the hypothermia group, while and 6 of 12 survived in the normothermia group (p=0.64). Intestines of the 72 h survivors were macroscopically normal. In rats that died during phase III, total gut scores did not differ statistically between the groups (1.2+/-0.6 versus 1.0+/-0.9). CONCLUSION: Brief resuscitative hypothermia of 60 min duration induced immediately with reperfusion after HS did not improve survival in this model.
BACKGROUND: In head injury patients, a decrease in the serum ionized magnesium (iMg) concentration is considered to be related to the severity of the injury, however, this phenomenon is still not completely understood. The cerebrospinal fluid (CSF) iMg concentration has not been well documented under such conditions and, moreover, its normal value has not yet been established. We hereby intended to investigate the role of the iMg concentration and other parameters in both the serum and CSF of head injury patients and identify any relationship with other parameters. MATERIALS AND METHODS: The subjects consisted of head injury patients without any other serious injuries. Ten healthy volunteers were selected as control subjects. Arterial blood and CSF specimens were simultaneously obtained and measured. We measured the Glasgow Coma Scale scores (GCS), the intracranial pressure (ICP), pH, po2, pco2, sodium, potassium, iCa, iMg, glucose, lactate, urea nitrogen. All data are expressed as the mean+/-SD and the units of iMg and iCa (corrected under pH 7.40) are given in mmol/L. RESULTS: In the healthy subjects, the iMg concentration in the serum/CSF was 0.48 +/- 0.02 / 0.66 +/- 0.14, and iCa was 1.14 +/- 0.05 / 0.94 +/- 0.07. The GCS of the 15 head injury subjects at examination was 8.7 +/- 4.5. When the subjects were divided into 3 groups according to the GCS level (3 and 4, 5-8, and > or =9) at the time of examination, the serum iMg concentration was thus found to be related to the severity of injury based on the GCS level (p = 0.028), but not the CSF iMg concentration (p = 0.89). No relationship was observed between the iMg concentration in the serum and CSF when all specimens were compared, but an extremely close correlation was seen in the group with GCS 3 and 4 (p < 0.0001, r = 0.995), although no such correlation was seen in the other 2 groups (p = 0.12, r = -0.56 in the group with GCS 5-8, and p = 0.26, r = -0.35 in the group with GCS > or = 9). There was a significant correlation between the serum iMg and iCa (p = 0.0093, r = 0.47), and also between the CSF iMg and iCa concentrations (p < 0.0001, r = 0.67). CONCLUSION: The serum iMg concentration has been suggested to possibly affect the neurologic state through CSF iMg in patients with the most severe head injury. In patients with moderate or mild head injuries, however, the ionized magnesium concentration is also probably associated with the degree of neurologic deficit based on the ionized calcium level. The CSF and serum ionized magnesium dissociation may thus result from the slow movement of ionized magnesium through the blood brain barrier.
A 17-year-old man presented with sleeping tendency, tenderness of the back of the neck, and left upper monoplegia after a motorcycle accident. Three-dimensional computed tomography on the 2nd hospital day clearly revealed a type I odontoid fracture. His injuries were treated conservatively and he was discharged on the 60th hospital day, with sequelae due to the cervical root avulsion injuries. Type I odontoid fracture is rare and may be caused by coronal distraction of the head and neck area.
A 50-year-old female who had a past history of non-treated hypertension, demonstrated a coma on arrival. CT revealed a high density lesion measuring 23 mm in transverse diameter and 15 mm in height at the ventral mid pons without breaking into a fourth ventricle or extending to the midbrain. She required mechanical ventilation support. Her consciousness improved on the 2nd hospital day. She showed tetra-plegia, which was especially dominant on her right side. Her symptoms gradually improved until she could stand and she was eventually discharged on the 41st hospital day. At 90 days after the initial presentation, an enhanced head MRI showed the absorption of the hematoma and no existence of any vascular malformation was observed. We herein report a case who dramatically recovered from a hypertensive pontine hemorrhage, despite the fact that she demonstrated several risk factors for a poor prognosis. The fact that the size of the hematoma was not so huge, and the location of the hematoma spared both the ascending reticular activating system and the nuclei, may explain the favorable outcome in this case.
OBJECTIVE: To clarify the clinical characteristics in organophosphate poisoning patients who require prolonged mechanical ventilation (PMV). MATERIAL AND METHODS: We reviewed the medical records of 15 adults organophsophate poisoning patients who admitted to our intensive care unit between Junuary, 1995, and December, 2004. The patients were divided into two groups: a PMV group requiring mechanical ventilation for more than 1 week (n=7) and a non PMV group (n=8), and various factors relating to PMV were compared between the two groups. RESULTS: The mean value of mechanical ventilation days was 16 +/- 6 days for the PMV group, which was significantly greater than 1 +/- 1 days for the non PMV group (p < 0.01). There were no statistical differences in the physical findings such as Japan Coma Scale, vital signs, and salivation and/or diarrhea, and in the treatments such as gastric lavage, administration of activated charcoal, and intravenous administration of pralidoxim and/or atropine on admission between the groups. The intermediate syndrome developed in 5 patients of the PMV group during their hospital course, whereas in no patient of the non-PMV group (p < 0.05). Hospital length of stay was 35 +/- 7 days in the PMV group, comparing with 11 +/- 11 days in the non-PMV group (p < 0.01). All patients of both groups survived and all but one patient returned to pre-hospital activities of daily living. CONCLUSIONS: Organophosphate poisoning patients requiring PMV had a higher incidence of the intermediate syndrome, but had similar mortality and morbidity compared with patients without PMV.
OBJECTS: To analyze the relationship between stress hormones (arginine vasopressin (ADH), adrenocorticotropic hormone (ACTH) and cortisol and the outcome of patients resuscitated after cardiopulmonary arrest (CPA). METHODS: Thirty-six patients were enrolled in this study. In 36 of the resuscitated cases, 27 were non-survivors and 9 survived. The survival group was defined as cases either in a persistent vegetative state, with some disability or good recovery 1 month after return of spontaneous circulation (ROSC). The non-survival group was defined as cases who died within 1 month. RESULTS: The plasma ADH and ACTH levels and the serum cortisol levels in both the surviving and the non-surviving patients were 82.3+/-74.5 and 149.6+/-135.4 (pg/ml), 239.7+/-327.4 and 282.4+/-553.0 (pg/ml), 34.1+/-11.2 and 19.0+/-12.8 (g/ml) (mean+/-S.D., respectively). The plasma ADH and ACTH levels showed no significant difference between the two groups. The serum cortisol levels were significantly higher in survivors than in the non-survivors (P=0.029). We also used the receiving-operating characteristics (ROC) curves to evaluate the optimal cutoff value of the concentration of serum cortisol as a predictive maker of non-surviving patients. The cutoff value of 16.7 g/ml for the concentrations of serum cortisol was a 1.00 positive predictive value and a 1.00 specificity at a 0.519 negative predictive and a 0.409 sensitivity for predicting non-surviving patients. The area under the ROC curve was calculated to be 0.858 at a prevalence of 0.58. The plasma ADH levels correlated significantly and positively with the plasma ACTH levels (r=0.516, P<0.0010). CONCLUSIONS: We concluded that the serum cortisol levels were significantly higher in survivors than in non-survivors resuscitated after CPA.
OBJECTIVE: The purpose of this study was to examine whether microwave tissue coagulation (MTC) therapy is capable of stopping bleeding from severe liver injury in pigs. METHODS: Ten pigs (38 +/- 4 kg) underwent a 30-mL/kg isovolemic exchange transfusion with 3% low-molecular-weight dextran to produce dilutional coagulopathy, and then a through-and-through laceration injury measuring approximately 8 cm in length was induced in the right hepatic lobe. Immediately after inflicting the injury, the animals were randomly divided into two groups: Group A (n = 5, MTC was repeated along the liver laceration at intervals of 2.0 cm with manual compression) or Group B (n = 5, the injured lobe was manually compressed without MTC therapy for 1 minute). All animals received lactated Ringer's solution to maintain the mean arterial pressure at 75 mm Hg for 1 hour after the abdominal closure. The intraperitoneal blood loss, mean arterial pressure, volume of lactated Ringer's solution, and hematologic variables were compared between the groups. For further laboratory evaluation, three additional experimental animals were treated with the MTC therapy after inflicting the injury and then were allowed to survive for 14 days. RESULTS: Mean arterial pressure declined from a mean value of 88 +/- 10 mm Hg (range, 75-107 mm Hg) to 62 +/- 3 mm Hg (range, 50-75 mm Hg) after the induction of liver injury. The total blood loss in Group A was 192 +/- 58 g (range, 120-250 g), which was lower (p < 0.01) than that of 448 +/- 138 g (range, 260-650 g) in Group B. The resuscitation fluid volume of Group A animals was 304 +/- 204 mL (range, 100-600 mL), which was smaller (p < 0.01) than that of 1,320 +/- 654 mL (range, 900-2,250 mL) in Group B. At 14 days, all three animals that were treated in the additional study were found to be in good health. Their necropsies showed no evidence of an intrahepatic abscess, hematoma, or biloma. CONCLUSION: MTC therapy was thus found to provide simple, rapid, and definitive hemorrhage control in cases of severe liver injury without the need for reoperation.
PURPOSE: We investigated blunt traumatic out-of-hospital cardiopulmonary arrest patients whether any clinical differences between with and without head injury existed or not. METHODS: A retrospective chart review of 332 blunt traumatic out-of-hospital cardiopulmonary arrest cases that had been transported to our hospital between January 1980 and April 2003. They were divided into two groups, head injury (HI, n = 175) and non-head injury (NHI, n = 157). RESULTS: There were no significant differences between the groups with respect to sex, age, mechanism of injury, witnessed arrest, bystander cardiopulmonary arrest, value of hemoglobin, value of base excess, and electrocardiogram on arrival. Averaged total abbreviated injury scale in the HI was greater than in the NHI, however return of spontaneous circulation in the HI was more frequent than in the NHI. Survival discharge rate was under 2% and good recovery case was none in the two groups. CONCLUSIONS: Among lethal blunt traumatic injuries, there were no different backgrounds between with and without head injury. The return of spontaneous circulation in the blunt traumatic patients with head injury became higher than without head injury, however the outcomes were similarly extremely poor.
OBJECTIVE: To examine whether induced hypothermia could prolong short-term survival after volume-controlled hemorrhagic shock (HS). MATERIALS AND METHODS: Fifteen pigs with systemic heparin underwent blood withdrawal of 30 ml/kg over 15 min under spontaneous breathing with halothane anesthesia. The pigs were divided into three groups of five pigs each: Group 1, hemorrhage plus hypothermia with extracorporeal shunt circulation (ECSC); Group 2, hemorrhage plus normothermia with ECSC; and Group 3, hemorrhage alone. For Groups 1 and 2, arteriovenous ECSC was performed for 20 min during HS. The re-infused shunt blood was cooled down to approximately 15 degrees C in Group 1, whereas it was returned at 37.5 degrees C in Group 2. The pigs in Group 3 had no ECSC and were left at room temperature. All pigs were observed until their death or for a maximum of 240 min. RESULTS: The mean pulmonary artery temperature (T(pa)) of Group 1 animals decreased to 34.5 degrees C at 15 min after the initiation of ECSC, and thereafter remained at 35.5 degrees C after undergoing ECSC. The T(pa) values for Groups 2 and 3 animals remained at 37.5 degrees C throughout the experiment. All five pigs in Group 1 survived until 240 min, whereas all pigs in Group 2 and 3 of five pigs in Group 3 died before 215 min after blood withdrawal. A life table analysis revealed significantly increased survival in Group 1 compared with Group 2 (P<0.01) and Group 3 (P<0.05). CONCLUSIONS: In lightly anesthetized pigs during volume-controlled HS, induced hypothermia may prolong their short-term survival for reasons that remain to be clarified.
The aim of this study was to examine the changes in the tissue Cu/Zn- and the Mn-SOD contents and gene expression following mild and severe burns in a rodent burn model. Thirty-eight male Wistar rats, weighing 208-278g, were divided into a sham burn group and two burn groups, with one receiving burns to 35% of the body surface and the other to 60%. Twenty animals of the burn groups were monitored daily for 7 days after injuries to examine survival. Six animals in the sham, 35 or 60% burn group were sacrificed at 3h postburn, and the blood, lungs and kidneys were collected for a biological analysis. The Cu/Zn- and Mn-SOD contents of the tissue and plasma specimens were measured using ELISA. The mRNA expressions of Cu/Zn- and Mn-SOD were determined by a Northern blot analysis. The survival rate of the 60% burn group for 7 days was 30%, whereas the survival rate of the 35% burn group was 100%. The mRNA expressions of Mn-SODs in the lung and the kidney were significantly higher in the 60% burn group than in 35% burn or sham burn group, as was the mRNA expression of lung Cu/Zn-SOD. Nevertheless, the tissue SOD contents in the 60% burn group (mortality 70%) did not exceed those in the 35% group. Based on these findings, tissue SOD synthesis is thus suggested to be inhibited in lethal burns in spite of a strong mRNA expression of SOD.
Explore the source record for details and available documents.
OBJECTIVE: To test our hypothesis that during lethal uncontrolled hemorrhagic shock (UHS) in rats, mild hypothermia of either 36 or 34 degrees C would prolong the survival time in comparison with normotherma of 38 degrees C. METHODS: Twenty-four rats were lightly anesthetized with halothane and maintained spontaneous breathing. UHS was induced by blood withdrawal of 2.5 ml/100 g over 15 min, followed by 75% tail amputation. Immediately after the tail cut, the rats were randomly divided into three groups (eight rats for each); normothermic Group 1 (control, rectal temperature 38 degrees C), and mild hypothermic Groups 2 (36 degrees C) and 3 (34 degrees C). Hypothermia was induced and maintained by body surface cooling. The rats were then observed without fluid resuscitation until their death (apnea and no pulse) or for a period of 240 min maximum. RESULTS: The rectal temperature was cooled down to 36 and 34 degrees C in 5 and 10 min, respectively. The mean survival time, which was 76+/-26 min in the control group (38 degrees C), was nearly doubled by mild hypothermia, 178+/-65 min for Group 2 (36 degrees C) (P<0.01 vs. control) and 144+/-54 min for Group 3 (34 degrees C) (P<0.05 vs. control) (no significant difference between Group 2 and 3). Additional blood losses from tail stumps were not significantly different among the three groups. CONCLUSION: Mild hypothermia of either 36 or 34 degrees C prolongs the survival time during lethal UHS in rats.
OBJECTIVE: The purpose of this study was to examine whether cold fluid infusion could rapidly decrease the core temperature and prolong survival during uncontrolled hemorrhagic shock in pigs. METHODS: Fourteen pigs under light halothane anesthesia and spontaneous breathing underwent initial blood withdrawal of 25 mL/kg over 15 minutes, followed by uncontrolled hemorrhage (5-mm aortotomy). Immediately after the aortotomy, the pigs were randomized to receive 500 mL lactated Ringer's solution at either 4 degrees C (group 1, n = 7) or 37 degrees C (group 2, n = 7) over 20 minutes through the internal jugular vein and observed until their death or for a maximum of 240 minutes. RESULTS: The pulmonary artery temperature of group 1 decreased to 35.5 degrees +/- 0.3 degrees C after the infusion, then remained at 35.5 degrees C during the observation period. Pulmonary artery temperature values of group 2 remained at around 37.5 degrees C throughout the experiment. The mean survival time was 220 +/- 45 minutes in group 1 versus 136 +/- 64 minutes in group 2 (p < 0.05, life table analysis). The additional intraperitoneal blood loss of group 1 was similar to that of group 2 (9 +/- 4 g/kg vs. 10 +/- 5 g/kg). CONCLUSION: In lightly anesthetized pigs during uncontrolled hemorrhagic shock, infusion with 4 degrees C lactated Ringer's solution (which seems to be feasible in the clinical setting) decreases the core temperature rapidly and prolongs survival.