Comparison of two methods for enumerating malaria parasites in thick blood films

We evaluated the risk of brain tumor occurrence in relation to previous head injury in a population-based case-control study of 540 children with a primary brain tumor and 801 control children. The risk of a brain tumor among children with a previous head injury that resulted in medical attention was slightly elevated when compared with children with no reported head injury [odds ratio (OR) = 1.4; 95% confidence limits (CL) = 1.0, 1.9]. This effect was stronger when we restricted the head-injured group to the few children with loss of consciousness (OR = 1.6; 95% CL = 0.6, 3.9) or an overnight admission to a hospital (OR = 1.7; 95% CL 0.7, 4.6), relative to those with no head injury. We observed no appreciable association between brain tumor occurrence and birth injury involving the head or a forceps delivery. Among the few children with either a birth injury or forceps delivery and a subsequent head injury, we observed approximately twofold elevations in risk. The OR was 2.6 (95% CL = 1.1, 6.9) for those with a birth injury and subsequent head injury, relative to those with neither a birth injury nor head injury. Our results provide only weak evidence in support of head injury as an etiologic agent for brain tumor occurrence in children, although most of our exposed group had only mild head injury.     

Clinical studies on renal trauma

A total of 18 kidneys in 17 patients with renal trauma were treated at the Department of Urology, Mitoyo General Hospital between April 1991 and August 1997. Patients were between 10 and 88 years old (median; 52). Eleven of them were male and 6 were female. The main cause of injury was a traffic accident in 11 cases (64.7%), which was similar in tendency to previous reports in this country. According to the Classification of Renal Injury by the Japanese Association for the Surgery of Trauma in Japan, there were 8 cases (47.1%) of Type I (sub-capsular injury) and Type II (superficial injury) that was classified a minor injury, and there were 9 cases (52.9%) of Type III (deep injury), Type IV (pedicle injury) and open injury that was classified as a major injury. Surgical treatment was performed in 8 cases (47.1%), which were all classified as a major injury. Posttraumatic plasma lactate dehydrogenase (LDH) was elevated immediately in case of major injury in comparison with a case of minor injury. Serum LDH may be useful as a parameter of the degree of renal trauma.     

The role of head injury in cognitive functioning, emotional adjustment and criminal behaviour

In two investigations, 50% of non-violent convicted felons, who avoided incarceration by participating in a day reporting programme, reported a prior history of head injury and current problems in cognitive and emotional functioning. Only 5% of a college sample in the first investigation and 15% of a community sample in the second investigation reported prior head injury. In a third investigation, 83% of felons who had reported a history of head injury also reported a date for their head injury that preceded the date of their first encounter with law enforcement. Some participants reported no trouble with the law until after experiencing a head injury that occurred in their late thirties. Considering the research reported here and elsewhere in the literature, it appears that many serious crimes follow a head injury. One implication of the findings reported here is that many crimes might not occur if people with head injury were given prompt and comprehensive treatment after the injury.     

Solid viscus injury predicts major hollow viscus injury in blunt abdominal trauma

BACKGROUND: As nonoperative management of blunt abdominal trauma has become more popular, reliable models for predicting the likelihood of concomitant hollow viscus injury in the hemodynamically stable patient with a solid viscus injury are increasingly important. METHODS: The Pennsylvania Trauma Systems Foundation registry was reviewed for the period from January 1992 to December 1995 for all adult (age > 12 years) patients with blunt trauma and an Abbreviated Injury Scale (AIS) score > or = 2 for a solid viscus (kidney, liver, pancreas, spleen). Patients with an initial systolic blood pressure < 90 mm Hg were excluded. Hollow viscus injuries included only lacerations or perforations of the gallbladder, gastrointestinal tract, or urinary tract. RESULTS: In the 4-year period, 3,089 patients sustained solid viscus injuries, 296 of whom had a hollow viscus injury (9.6%). The mean age was 35.6 years, mean Injury Severity Score was 22.2, and mean Revised Trauma Score was 7.3; 63.3% of the patients were male. A solitary solid viscus injury occurred in 2,437 patients (79%), 177 of whom (7.3%) had a hollow viscus injury. The frequency of hollow viscus injury increased with the number of solid organs injured: 15.4% of patients with two solid viscus injuries (n = 547) and 34.4% of patients with three solid viscus injuries (n = 96) suffered a concomitant hollow viscus injury (p < 0.001 vs. one organ). A hollow viscus injury was 2.3 times more likely for two solid viscus injuries and 6.7 times more likely for three solid viscus injuries compared with a solitary solid viscus injury. For solitary solid viscus injury, the frequency of hollow viscus injury varied little with increasing AIS score (AIS score 2, 6.6%; AIS score 3, 8.2%; AIS score 4, 9.2%; AIS score 5, 6.2%) (p = 0.27 between groups), suggesting that the incidence of hollow viscus injury is related more to the number of solid visceral injuries than the severity of individual organ injury. Also, when the sum of the AIS scores for solid viscus injuries was <6, the mean rate of hollow viscus injury was 7.8%. This increased to 22.8% when the sum of the AIS scores for solid viscus injury was > or =6 (p < 0.001). A pancreatic injury in combination with any other solid viscus injury had a rate of hollow viscus injury of >33%. CONCLUSION: A model of organ injury scaling predicted hollow viscus injury. Multiple solid viscus injuries, particularly pancreatic, or abdominal solid viscus injuries with an AIS score > or = 6, were predictive of hollow viscus injury. Identification of these injury patterns should prompt consideration for early operative intervention.     

Defining assessment parameters in dual injuries: spinal cord injury and traumatic brain injury

Assessment parameters for muscle testing in the individual with a spinal cord injury (SCI) have been clearly defined by the American Spinal Injury Association (ASIA). However, the ASIA standard requires the individual's participation in reporting sensory information and he/she must be able to perform specific tasks to complete the examination. In an individual with a dual injury, a SCI and a traumatic brain injury (TBI), neurological assessment can be impeded by the individual's inability to participate in the exam. Assessment needs to incorporate both cognitive and physical parameters that will appropriately assess both injuries. This article reviews the assessment parameters for both spinal cord injury and traumatic brain injury and provides assessment guidelines for bedside evaluation of functional ability. In addition, a review of the biomechanics of injury will provide a model for understanding dual injury.     

Characterization of the early events in vitamin C and K3-induced death of human bladder tumor cells

BACKGROUND: Water under high pressure can produce vaginal injury. Previous reports suggest that postmenarcheal maturation and the presence of a vaginal foreign body contributed to water slide injuries in women. METHODS: A case of a vaginal injury from a water slide in a premenarcheal patient is presented. A literature review of water-related vaginal injuries in adults and children compares the mechanism of injury with that previously reported. RESULTS: The patient underwent operative repair of her injury. CONCLUSIONS: Vaginal injury in premenarcheal patients may result from a water slide. The emergency physician must be aware of this potential injury mechanism and the need for complete examination under anesthesia when vaginal bleeding is present.     

Cognitive and motor functioning in Parkinson disease: subjects with and without questionable dementia

We evaluated the data of the National Collegiate Athletic Association Injury Surveillance System on collegiate wrestling with a focus on musculoskeletal injuries. Over 800,000 athlete-exposures during an 11-year period compose these data. Findings particular to wrestling and a comparison with other collegiate sports are included. Collegiate wrestling had a relatively high rate of injury at 9.6 injuries per 1000 athlete-exposures. It was second to spring football in total injury rate. Most injuries in this study were not serious, with 6.3% resulting in surgery and 37.6% resulting in a week or more off from wrestling. There was only one catastrophic, nonfatal injury. The knee, shoulder, and ankle were the most commonly injured regions, and injuries to them were often the more serious. Sprains, strains, and contusions were the most common injury types. Takedowns and sparring were the most common activities at the time of injury. Mechanism of injury was evaluated; rotation about a planted foot and contact with environmental objects were identified as areas needing further attention. Illegal action accounted for only 4.6% of injuries in competition. Competition had a significantly higher injury rate than practice, but the injury profiles of these two areas showed both to be equally important. The preseason and regular season had higher injury rates than the postseason, but, again, the injury profiles of these periods were similar. Injury percentages were similar among the 10 weight classes.     

SB209670, a potent endothelin receptor antagonist, prevents or delays axonal degeneration after spinal cord injury

We developed a rat spinal cord transection injury model and investigated whether endogenous endothelin takes part in axonal degeneration after injury, by using a potent nonselective endothelin receptor antagonist, SB209670. Light microscopic analysis showed that axonal degeneration of the spinal cord was clearly observed one week after injury, supported by immunohistochemical study with anti-neurofilament antibody. Electron microscopic observation showed enlargement and shrinking of spinal axons in the injured sites one week after injury. Application of SB209670 to the lesion sites markedly inhibited axonal damage after injury. These results suggest that endogenous endothelin plays a role in axonal degeneration after spinal cord injury and that SB209670 prevents or delays the axonal degeneration after CNS damage.     

Relationship of trauma patient volume to outcome experience: can a relationship be defined?

OBJECTIVES: Five years experience recorded in a multi-institutional pediatric trauma registry was analyzed to define the relationship between case volume and outcome as measured by mortality. METHODS: A total of 30,930 records with complete data were categorized by contributing hospital. Patients with fatal injury as indicated by an injury severity score of 75 or any abbreviated injury scale of 6 were excluded. Each center's experience was stratified by injury severity using injury severity score > or = 15 as indicative of severe injury. Centers were then classified as low volume (LV, 100-500 cases), mid volume (MV, 501-1,000 cases), or high volume (HV, > 1,000 cases). Proportion of patients with severe injury (injury severity score > 15) and mortality were compared among groups using the chi(2) test with significance accepted at p < 0.05. Using the Pediatric Risk Indicator to adjust for mortality risk, the combined hospital experience of each volume group was further analyzed to assess performance with specific levels of increasing injury severity. RESULTS: Findings demonstrated a trend of increasing mortality with increasing volume, despite a consistent proportion of severe injury. Risk adjusted mortality for each volume class indicates best outcome in the mid level group. CONCLUSIONS: Regardless of overall volume of patients encountered, there is a consistent proportion of severe injury. The increasing mortality with the most severe injuries seen in the high volume centers may reflect overdemand on resources.     

The neuronal cytoskeleton is at risk after mild and moderate brain injury

Recent studies have described alterations in cytoskeletal proteins such as microtubule-associated protein 2 (MAP-2) and neurofilament (NF) resulting from moderate and severe experimental brain injury; however, few have investigated the consequences of mild injury, which is associated clinically and experimentally with cognitive dysfunction and neuronal damage. To contrast cytoskeletal changes within 7 days following mild injury with those following moderate injury, we subjected anesthetized, adult rats to mild (1.1-1.3 atm) or moderate (2.3-2.5 atm) lateral fluid percussion brain injury or sham injury. Rats were sacrificed at 6 h (n=4 mild; n=4 moderate; n=2 sham), 24 h (n=4 mild; n=4 moderate; n=1 sham), or 7 days (n=5 mild; n=4 moderate; n=1 sham) following injury, and immunohistochemistry was performed for MAP-2 and NF. Both mild and moderate injury produced notable cytoskeletal changes in multiple brain regions; however, mild injury generally resulted in a lesser degree of MAP-2 and NF loss over a smaller spatial extent. When compared to moderately injured animals, animals subjected to mild injury showed substantially delayed MAP-2 and NF alterations within the cortex and hippocampal dentate gyrus and no evidence of MAP-2 loss in the hippocampal CA3 region. While mild and moderate injury resulted for the most part in similar patterns of axonal injury, tissue tears in the fimbria and loss of NF immunoreactivity in regions containing injured axons were only observed following moderate injury. Elucidating the effects of modulating injury severity may yield insight into the mechanisms involved in traumatic damage to the cytoskeleton and guide future treatment strategies.     

Late displacement of a fracture dislocation at the lumbosacral junction. A case study

STUDY DESIGN: This is a retrospective single-patient case report with a literature review. OBJECTIVE: To report on an uncommon injury: traumatic fracture-dislocation of the lumbosacral junction with delayed displacement. SUMMARY OF BACKGROUND DATA: Only 31 cases of traumatic fracture-dislocation of the lumbosacral junction were found in the English literature. Only three previous reports refer to this injury occurring with a posterior displacement. This is the first report of this type of injury displacing in a delayed manner. METHODS: Chart review. RESULTS: Open reduction, Arbeitsgemeinschaft fur Osteosynthesefargen instrumentation, and interbody fusion resulted in a satisfactory clinical result with no neurologic impairment. CONCLUSIONS: The present study reports a very rare injury consisting of traumatic dislocation of the lumbosacral joint, presenting with displacement 2 months after injury. The patient was treated successfully with surgery even though the injury displaced in a delayed fashion.     

Geriatric psycho-social history outline

The outcome o,f marriages contracted after spinal cord injury suffered by males was examined via the questionnaire method. Of those whose first marriage occurred after their injury, the divorce rate was 24.4%. Of those whose were married prior to injury and then remarried following injury, 16.4% were divorced. If all post-injury marriages are considered, the divorce rate is 23.1%. This is close to the divorce rate of the United States as a whole. The outcome of post-injury marriages was also examined with respect to time since injury, level of injury, presence of post-injury children, and post-injury education and employment. Particular attention was given to those males who had never been married prior to their injury.     

Apoptosis as a mechanism of neuronal cell death following acute experimental spinal cord injury

The complex biochemical interactions following acute spinal cord injury have undergone considerable investigation recently. Progress has been made in discovering both primary and secondary injury cascades that combine to produce the ultimate neurologic insult. Traditionally, neuronal and supporting cell death following spinal cord injury have focused on necrotic death pathways resulting passively from the actual mechanical tissue damage and inflammatory processes which follow. However, the occurrence of programmed apoptotic cell death which is an actively mediated cellular process may occur following acute spinal cord injury and, if present, may play a role in the ultimate neurologic insult. In this study, we document a chronologically-specific course of apoptotic cell death by the TUNEL assay technique following an acute experimental spinal cord injury in the rat model. In this manner, apoptotic cell death following acute spinal cord injury may play a pivotal role in the secondary injury cascade which produces the ultimate neurologic insult and may allow potential for mediating neuronal survival via anti-apoptotic factors such as the protooncogene Bcl-2.     

Effect of glucose administration on contusion volume after moderate cortical impact injury in rats

Previous studies had shown that pre- and postinjury glucose administration increased brain injury caused by a mild cortical impact injury only when the traumatic injury was complicated by a secondary ischemic insult. The purpose of this study was to examine the effect of pre- and postinjury glucose administration on a more severe cortical impact injury, where primary ischemia occurs at the site of the impact. Long Evans rats who were fasted overnight and anesthetized with isoflurane were subjected to a 5-m/sec, 2.5-mm impact injury. The animals were randomly assigned one of the following treatments: (1) 2.2 g/kg glucose in 4 ml of saline, 20 min prior to injury; (2) 2.0 g/kg glucose in 4 ml of saline, 20 min after injury; or (3) 4 ml of saline either 20 min before injury or 20 min after the injury. At 2 weeks, the animals were sacrificed and the brains were examined for contusion volume and for neuronal loss in CA1 and CA3 regions of the hippocampus. Contusion volume was increased from a median value of 23 mm3 in the saline-infused animals to 34 mm3 in the preimpact glucose infusion animals (p=0.005). Postimpact glucose infusion had no effect on contusion volume. Neuron density in CA1 and CA3 regions of the hippocampus was similar in all three treatment groups. These studies support the hypothesis that glucose administration adversely affects experimental traumatic brain injury in those circumstances where the trauma is complicated by primary cerebral ischemia, such as around cortical contusions.     

Apoptosis in substantia nigra following developmental hypoxic-ischemic injury

We have previously observed that either hypoxic-ischemic or excitotoxic striatal injury during development is associated with a reduction in the adult number of dopaminergic neurons in the substantia nigra. This decrease occurs in the presence of preserved striatal dopaminergic markers and in the absence of direct nigral injury. We have also observed that natural cell death, with the morphology of apoptosis, occurs in the substantia nigra, and that there is an induced apoptotic cell death event following early striatal excitotoxic injury. We now report that forebrain hypoxic-ischemic injury is also associated with an induced cell death event in the substantia nigra, with both morphological and histochemical features of apoptosis. Induced apoptotic cell death occurs in immunohistochemically defined dopaminergic neurons. While the mechanisms for this induced cell death are not yet known, in the case of the pars compacta it may be related to the loss of normal striatal target-derived developmental support. Since dopaminergic neurons are postmitotic at the time of the injury, we conclude that this induced cell death is responsible for the diminished adult number of dopaminergic neurons. We also conclude that hypoxic-ischemic injury to the developing brain in general causes not only direct, necrotic injury to vulnerable regions, but also induced apoptotic death at remote sites. The significance of this finding is that apoptosis is a distinct death mechanism, with unique regulatory pathways, which can potentially be modified by approaches different from those which might influence cell death in regions of direct injury. In view of the present finding that apoptosis can occur in the setting of hypoxic-ischemic injury, and our previous work demonstrating its occurrence following excitotoxic injury, it seems likely that it may occur following other forms of injury to the immature brain in which excitotoxic injury plays a role, such as seizures, head trauma and hypoglycemia.     

Alterations in temporal/spatial distribution of GFAP- and vimentin-positive astrocytes after spinal cord contusion with the New York University spinal cord injury device

Astrocytes become reactive as a result of various types of lesions and upregulate 2 intermediate filaments, glial fibrillary acidic protein (GFAP), and the developmentally regulated protein vimentin. Young female Sprague-Dawley rats were subjected to a spinal cord contusion at segment T10 using the New York University injury device. Animals were killed at 1, 2, 7, 14, and 30 days postinjury. Horizontal spinal cord sections spanning segments T7-T13 were assessed with antibodies to both intermediate filament proteins. The number of gray matter GFAP-positive astrocytes increased by 2 days postinjury, with segments adjacent (proximal) to the injury site showing greater responses than areas several segments away (distal). By 30 days following injury, astroglial cell numbers returned to normal levels. Vimentin-positive astrocytes also showed a graded proximal/distal response by 2 days following injury. Proximal regions remained significantly higher at 30 days following injury than control animals. Rostral/caudal changes were also evident, with regions caudal to the injury showing significantly higher numbers of vimentin positive astrocytes than those rostral, indicating that gray matter areas caudal to spinal cord injury may undergo more stress following spinal cord injury.     

Smooth muscle cell migration and matrix metalloproteinase expression after arterial injury in the rat

We have characterized matrix metalloproteinase expression in the rat carotid artery after two forms of arterial injury, balloon catheter denudation and nylon filament denudation. Gelatinolytic enzymes with molecular masses of 70 and 62 kD were produced constitutively in the rat carotid. Production of an 88-kD gelatinase was induced after balloon catheter injury, and proteinase production continued during the period of migration of smooth muscle cells from the media to the intima, from 6 hours to 6 days after balloon catheter injury. In addition, a marked increase in 62-kD gelatinolytic activity was observed between 4 and 14 days after arterial injury. Gelatinase activities (88 and 62 kD) were also increased after nylon filament denudation but were markedly less after this injury than after balloon catheter injury. These results suggested a correlation between gelatinase activity and smooth muscle cell migration after arterial injury. Administration of a metalloproteinase inhibitor after balloon catheter injury resulted in a 97% reduction in the number of smooth muscle cells migrating into the intima. Therefore, we hypothesize that gelatinase expression directly facilitates smooth muscle cell migration within the media and into the intima. These results suggest that gelatinases are involved in the vascular smooth muscle cell activation and neointimal formation that characterize arterial tissue remodeling after injury.     

Induction of glutamine synthetase expression after major burn injury is tissue specific and temporally variable

BACKGROUND: Major burn injury results in a translocation of amino acids from peripheral tissues to the abdominal viscera. Glutamine is a major participant in this event. Thermal injury causes a depletion of plasma and muscle glutamine pools as well as activation of proteolysis and release of glutamine from skeletal muscle. De novo synthesis of glutamine is regulated by the expression of the enzyme glutamine synthetase (GS). We studied the tissue-specific regulation of GS expression after thermal injury. METHODS: Burn injury of rats was produced by scalding of 25 or 40% of skin surface. In normal rats, four organs, including lung, muscle, kidney, and liver were assayed for relative GS messenger RNA content by Northern blotting 8 and 24 hours after 40% area burn. The effect of adrenalectomy on GS mRNA induction in muscle was assessed 24 hours after 25% area burn injury. RESULTS: GS mRNA levels were increased 2.3-fold in lung at 8 hours and 7.3-fold in muscle at 24 hours after burn injury. No appreciable increase in GS mRNA level was observed in kidney or liver. Muscle GS mRNA levels were lower than sham-operated controls in both burned and unburned adrenalectomized rats. However, adrenalectomy did not attenuate relative GS mRNA induction in muscle at 24 hours after burn injury. CONCLUSIONS: Burn injury causes an induction in GS mRNA levels in a tissue-specific fashion. Adrenalectomy greatly reduced GS mRNA levels, but did not completely block the induction of GS express in muscle after burn injury. This finding suggests that glucocorticoid hormones together with a unknown factor of nonadrenal origin influence this metabolic response to burn injury.     

Improved identification of coronary artery disease in patients with left bundle branch block by use of dobutamine stress echocardiography and comparison with myocardial perfusion tomography

The purpose of this report is to compare a computed tomography (CT) injury severity scale for hepatic and splenic injury with the following outcome measures: requirement for surgical hemostasis, requirement for blood transfusion and late complications. Sixty-nine children with isolated hepatic injury and 53 with isolated splenic injury were prospectively classified at CT according to extent of parenchymal involvement. Clinical records were reviewed to determine clinical outcome. Ninety-seven children (80%) were managed non-operatively without transfusion. One child with hepatic injury required surgical hemostasis, and 17 (25%) required transfusion of blood. Increasing severity of hepatic injury at CT was associated with progressively greater frequency of transfusion (P = 0.002 by chi 2-test). One child with splenic injury underwent surgery and eight (15%) required transfusion of blood. Splenic injury grade at CT did not correlate with frequency (P = 0.41 by chi 2-test) or amount (P = 0.35 by factorial analysis of variance) of transfusion. There was one late complication in the nonsurgical group. A majority of children with hepatic and splenic injury were managed non-operatively without requiring blood transfusion. The severity of injury by CT scan did not correlate with need for surgery. Increasing grade of hepatic injury at CT was associated with increasing frequency of blood transfusion. CT staging was not discriminatory in predicting transfusion requirement in splenic injury.     

Time course of changes in lactate and free fatty acids after experimental brain injury and relationship to morphologic damage

Regional levels of lactate and free fatty acids (FFA) were measured after lateral fluid percussion (FP) brain injury in rats. At 5 min after injury, tissue concentrations of lactate were elevated in the cortices and hippocampi of both ipsilateral and contralateral hemispheres. Whereas lactate levels had returned to normal by about 20 min after injury in the penumbra and contralateral cortices, their elevation persisted in the ipsilateral injured cortex and hippocampus for 24 h after injury. Increases in the levels of FFA (particularly stearic and arachidonic acids) were observed in the cortices and hippocampi of both ipsilateral and contralateral hemispheres at 5 min after injury; these levels returned to normal in only the penumbra and contralateral cortices by 20 min after injury. Increased amounts of palmitic and oleic acids were also found only in the injured left cortex and ipsilateral hippocampus at 20 min or later after injury. In general, these elevations persisted for as long as 6 to 24 h in the injured cortex and for 2.5 to 24 h after injury in the ipsilateral hippocampus. Histologic studies revealed a similar extent of damage in the cortex between 5 min and 24 h after injury, whereas damage in the CA3 region of the ipsilateral hippocampus increased during that period. These findings suggest a role for lactic acid and FFA, two secondary injury factors, in neuronal cell loss after brain injury.