Cardioinhibitory reflex due to a karate kick: a case report.

This article describes the case of a 17-year-old adolescent boy who received a foot kick in the trunk area from an expert in karate. He presented with immediate cardiocirculatory arrest. After a prolonged resuscitation, he was transferred to a hospital where he died 5 days later without ever regaining consciousness. Postmortem investigations including autopsy, radiology, histology, toxicology, and postmortem chemistry were performed that showed signs of multiple organ failure, an acute hemorrhage in the region of the celiac plexus, and signs of medical resuscitation. No preexisting disease, particularly those concerning the heart, was objectified. The cause of death was attributed to multiple organ failure after a prolonged cardiocirculatory arrest. Concerning the origin of the cardiac arrest, 2 hypotheses were considered-a cardioinhibitory reflex and a cardiac contusion (commotio cordis). Because of the presence of traumatic lesions in the celiac plexus, the first hypothesis was finally submitted. This case is reported because rare cases of sudden death from celiac reflex are described in the literature where it is almost impossible to find references with accurate documentation. The presented case confirms the importance of detailed documentation of the circumstances and postmortem investigations to establish a diagnosis of death due to cardioinhibitory reflex.

A cannabinoid type 2 receptor agonist attenuates blood-brain barrier damage and neurodegeneration in a murine model of traumatic brain injury.

After traumatic brain injury (TBI), inflammation participates in both the secondary injury cascades and the repair of the CNS, both of which are influenced by the endocannabinoid system. This study determined the effects of repeated treatment with a cannabinoid type 2 receptor (CB(2) R) agonist on blood-brain barrier integrity, neuronal degeneration, and behavioral outcome in mice with TBI. We also looked for the presence of a prolonged treatment effect on the macrophage/microglial response to injury. C57BL/6 mice underwent controlled cortical impact (CCI) and received repeated treatments with a CB(2) R agonist, 0-1966, or vehicle. After euthanasia at 6 hr or 1, 2, 3, or 7 days postinjury, brains were removed for histochemical analysis. Blood-brain barrier permeability changes were evaluated by using sodium fluorescein (NaF). Perilesional degenerating neurons, injury volumes, and macrophage/microglia cells were quantified by stereological methods. Rota-rod and open-field testing were performed to evaluate motor function and natural exploratory behavior in mice. 0-1966 Treatment resulted in a significant reduction in NaF uptake and number of degenerating neurons compared with the vehicle-treated group. 0-1966-Treated mice demonstrated improvement on rota-rod and open-field testing compared with vehicle-treated mice. These changes in CCI mice treated with 0-1966 were associated with a prolonged reduction in macrophage/microglia cell counts. In conclusion, repeated treatments with a CB(2) R agonist, 0-1966, result in attenuated blood-brain barrier disruption and neuronal degeneration. In addition, repeated treatment with 0-1966 shows prolonged treatment effects on behavior and the macrophage/microglia cell response over several days.

The life-saving effect of hyperbaric oxygenation during early-phase severe blunt chest injuries.

The effect of hyperbaric oxygenation (HBO2) on survival during the early phase of severe blunt chest injury (BChI) has not been elucidated. Our aim was to investigate this effect on human victims of BChI. We monitored cardiac index (CI), stroke volume index (SVI), PaO2 and PaO2/FiO2 in 18 victims treated conventionally, and 8 victims treated under combined conventional and HBO2 treatment. Out of the 18 victims, 4 survived (Group A) and 14 died (Group B). Another 8 victims, in Group C, received HBO, and all survived. Human victims showed marked reductions in all cardiorespiratory values during the first 24 h. Group B persistently tended towards a decrease in SVI, PaO2/FiO2 and PaO2, eventually reaching fatal levels. The survivors developed a cardiorespiratory function characterized by a tendency towards recovery of all monitored parameters, more notable in Group C, which showed an earlier and more significant normalization vs. Group A (P<0.01). Our clinical data suggest that the earliest possible HBO2 treatment after severe blunt trauma can significantly enhance victims' survival.

Noninvasive hemodynamic monitoring for combat casualties.

The aims of this study were to develop and to test a noninvasive hemodynamic monitoring system that could be applied to combat casualties to supplement conventional vital signs, to use an advanced information system to predict outcomes, and to evaluate the relative effectiveness of various therapies with instant feedback information during acute emergency conditions. In a university-run inner city public hospital, we evaluated 1,000 consecutively monitored trauma patients in the initial resuscitation period, beginning shortly after admission to the emergency department. In addition to conventional vital signs, we used noninvasive monitoring devices (cardiac index by bioimpedance with blood pressure and heart rate to measure cardiac function, arterial hemoglobin oxygen saturation by pulse oximetry to reflect changes in pulmonary function, and tissue oxygenation by transcutaneous oxygen tension indexed to fractional inspired oxygen concentration and carbon dioxide tension to evaluate tissue perfusion). The cardiac index, mean arterial pressure, pulse oximetry (arterial hemoglobin oxygen saturation), and transcutaneous oxygen tension/fractional inspired oxygen concentration were significantly higher in survivors, whereas the heart rate and carbon dioxide tension were higher in nonsurvivors. The calculated survival probability was a useful outcome predictor that also served as a measure of severity of illness. The rate of misclassification of survival probability was 13.5% in the series as a whole but only 6% for patients without severe head injuries and brain death. Application of noninvasive hemodynamic monitoring to acute emergency trauma patients in the emergency department is feasible, safe, and inexpensive and provides accurate hemodynamic patterns in continuous, on-line, real-time, graphical displays of the status of cardiac, pulmonary, and tissue perfusion functions. Combined with an information system, this approach provided an early outcome predictor and evaluated, with an objective individualized method, the relative efficacy of alternative therapies for specific patients.

Endogenous adenosine and secondary injury after chest trauma.

BACKGROUND: No previous studies have examined actions of adenosine or related compounds after blunt chest trauma, but we have shown that the prototype adenosine-regulating agent, acadesine (aminoimidazole carboxamide ribonucleotide [AICAR]), has multiple favorable anti-inflammatory actions after other forms of trauma, ischemia, hemorrhage, and sepsis; and that a progressive inflammatory response in the contralateral (uninjured) lung after unilateral blunt chest trauma is caused (in part) by activation and sequestration of circulating leukocytes (white blood cells [WBCs]). Thus, we hypothesized that AICAR would ameliorate WBC-dependent, secondary pathophysiologic changes after blunt chest trauma. METHODS: Mongrel pigs (28+/-1 kg, n = 21) were anesthetized, mechanically ventilated, and injured on the right chest (pulmonary contusion) with a captive bolt gun. Either AICAR (1 mg/kg + 0.2 mg/kg/min) or its saline vehicle were administered for a 12-hour period, beginning 15 minutes before injury. RESULTS: Injury caused a three- to fourfold increase in bronchoalveolar lavage (BAL) WBC counts, 10- to 20-fold increases in BAL protein, and 200% increases in lung edema as measured by wet-dry ratio (all p < 0.05), in both the injured (right) and the noninjured (left) lungs. With AICAR versus saline, BAL WBC counts, lung myeloperoxidase levels, and systemic hemodynamics were similar. However, the increases in BAL protein were attenuated by 30% to 50% (p < 0.14, NS) and edema was reduced (p < 0.05) in both lungs. Furthermore, oxygenation, hypercapnia, acidosis (all p < 0.05), and survival were improved (9 of 10 vs. 4 of 11, p < 0.04). CONCLUSION: Pretreatment with AICAR before experimental pulmonary contusion ameliorates the trauma-induced destruction of the alveolar capillary membrane, and attenuates the delayed secondary injury in the contralateral uninjured lung, by a mechanism that may be independent of leukocytes. Endogenous adenosine could have a role in the pathophysiologic response after blunt chest injury, with potential sites of action including the endothelium and alveolar macrophage. Adenosine-regulating agents may have therapeutic potential after blunt chest injury, but further studies are needed in clinically relevant models, with administration begun at the time of resuscitation.

Posttraumatic hypothermia reduces polymorphonuclear leukocyte accumulation following spinal cord injury in rats.

The present study addresses the effects of moderate posttraumatic hypothermia (32 degrees C) on the temporal and regional profile of polymorphonuclear leukocyte (PMNL) accumulation after traumatic spinal cord injury (SCI). We hypothesized that posttraumatic hypothermia would reduce the degree of inflammation by reducing PMNL infiltration. Rats underwent moderate spinal cord injury at T10 using the NYU impactor device. In the first study, the temporal profile of myeloperoxidase (MPO) activity (a marker of neutrophil accumulation) under normothermic (37 degrees C) conditions was determined. The animals were allowed to survive for 3 or 24 h, or 3 or 7 days after SCI. Spinal cords were dissected into five segments rostral and caudal to the injury site. Additional animals were studied for the immunocytochemical visualization of MPO. In the second study, rats were sacrificed at 24 h after a monitoring period of normothermia (36.5 degrees C/3 h) or hypothermia (32.4 degrees C/3 h) with their controls. In the time course studies, MPO enzymatic activity was significantly increased at 3 and 24 h within the traumatized T10 segment compared to controls. MPO activity was also increased at 3 h within the rostral T8 and T9 segments and caudal T11 and T12 segments compared to controls. At 24 h after trauma, MPO activity remained elevated within both the rostral and caudal segments compared to control. By 3 days, the levels of MPO activity were reduced compared to the 24-h values but remained significantly different from control. Neutrophils that exhibited MPO immunoreactivity were seen at 6 and 24 h, with a higher number at 3 days. PMNLs were located within the white and gray matter of the lesion and both rostral and caudal to the injury site. Posttraumatic hypothermia reduced MPO activity at 24 h in the injured spinal cord segment, compared to normothermic values. The results of this study indicate that a potential mechanism by which hypothermia improves outcome following SCI is by attenuating posttraumatic inflammation.

Cellular reactivity to mechanical axonal injury in an organotypic in vitro model of neurotrauma.

An in vitro model of traumatic brain injury is described that is based on organotypic cocultures (OTCs) of rat neocortex and thalamus connected by reciprocal axonal projections. Localized mechanical compression of this projection was inflicted with a mechanical device, and the effects on cell viability, axonal morphology, and protein expression levels were analyzed. Within 24 h after insult, major cell damage occurred in infragranular cortical layers containing the corticothalamic projection neurons and in thalamic regions adjacent to the mechanical impact as was assessed through the use of the vital stain Syto 21, and propidium iodide labeling. A small, but significant number of calretinin-positive interneurons in cortical and thalamic areas displayed symptoms of injury. Axonal elements, as revealed by neurofilament (NF-H/M) immunohistochemistry, in the corticothalamic transition zone displayed pathomorphological changes, such as axonal bulbs and swellings, already 4 h after insult. Densitometric analysis revealed that MAP-2a,b expression was not significantly changed within 4 h after injury. A significant reduction in MAP-2a,b amount was evident at 20 h after injury in thalamus (by 31.6%) and cortex (by 30%) maintained for 12 days in vitro (DIV), but not in OTCs aged 20 DIV. The axonally localized form MAP-2c significantly increased in cortex of 12-DIV OTCs at 4 and 20 h after insult (65.6% and 33.4%, respectively). MAP-2c levels in cortex of 20 DIV initially increased by 47.7% and declined below control values 20 h after injury. Thalamic areas revealed a delay in MAP-2c reactivity, in that expression was significantly elevated only at 20 h after injury (by 84.4% in 12-DIV and by 39.6% in 20-DIV OTCs, respectively). These data may reflect the regenerative ability of juvenile, but not of older neurons in response to mechanical axonal injury.

[Encephaloangioscintigraphy in the diagnosis of posttraumatic cerebral venous circulatory disorders]. / Entsefaloangiostsintigrafiia v diagnostike posttravmaticheskikh tserebral'nykh venoznykh distsirkuliatsii.

Encephaloangioscintigraphy performed in 30 patients with a closed craniocerebral trauma has shown simultaneous inhibition of the venous cerebral blood flow both in the vascular regions of the cerebral hemispheres and in the lateral sinuses indicating the common pathogenesis of disorders of the venous circulation in these parts of the circulatory bed. The most informative characteristic feature of the venous outflow is a period of RP half-life, determined on a radiocirculogram of the brain. The diagnostic efficacy of the above method in the detection of disorders of the venous circulation of the brain in some vascular regions provides an opportunity for a purpose-oriented use of adequate methods of reflexotherapy.

Thoracic injury potential of basic competition taekwondo kicks.

A major concern in competition taekwondo is the injury potential posed by many of the powerful kicks used. An investigation of the kinetics of four kicks frequently used in competition was performed with high speed video. Velocities were measured, and energy was calculated. Typical values for basic swing kicks were 15 ms-1 and 200 J. Basic thrust kicks possessed 45% less velocity but 28% more energy than swing kicks. Linkage models were developed to simulate the motion and kinetics of the kicking leg. Injury potential was evaluated through thoracic compression and viscous criterion models. These models predict a significant probability of serious injury with all kicks, with thoracic deflections from 3 to 5 cm and peak viscous tolerance values from 0.9-1.4 ms-1, when no protective body equipment is used.

[Short-latency brain stem evoked potentials to acoustic stimulation in closed craniocerebral trauma in children]. / Korotkolatentnye stvolovye vyzvannye potentsialy na akusticheskuiu stimuliatsiiu pri zakrytoi cherepno-mozgovoi travme u detei.

Twenty-six children with closed craniocerebral trauma (CCCT) of various severity were examined by recording short-latent stem-induced potentials in response to acoustic stimulation. Prognostical authenticity of the method in severe CCCT in children was established, which allowed reversible and irreversible disorders of brain them function to be distinguished. Studies in dynamics made it possible to follow the course of the pathological process and correct the applied therapy in time.