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At least 433 records · Page 24Linked to original sources
PubMed1988

Value of early operation in blunt testicular contusion with hematocele.

The use of ultrasound for evaluation of blunt testicular injury with hematocele allows contusion to be differentiated from rupture, and some authors advocate reserving surgical management for rupture. Our experience with the conservative management of 20 men with testicular contusion and hematocele was not encouraging. Of the patients 8 (40 per cent) required delayed exploration that involved orchiectomy in 3 (15 per cent) because of unresorbed hematoma or infection despite antibiotic use. In contrast, early surgical exploration in 19 patients reduced the morbidity and duration of disability, and resulted in an orchiectomy rate of 0.

Contusions↗
PubMed1993

Severe right ventricular contusion mimicking cardiac tamponade: the value of transesophageal echocardiography in blunt chest trauma.

Clinically, severe right ventricular contusion may mimic cardiac tamponade. We report two cases of suspected cardiac tamponade after blunt chest trauma in which the diagnosis of severe right ventricular contusion was made only by transesophageal echocardiography, avoiding unnecessary and hazardous pericardiocentesis. These cases illustrate the value of transesophageal echocardiography in diagnosing blunt chest trauma.

Adult↗
PubMed2000

Cytokine chemokine expression in contused rat spinal cord.

Spinal cord injury within the first few hours, is complicated by inflammatory mechanisms, including the influx of monocyte/macrophages as well as the activation of resident spinal microglia and astrocytes. Numerous studies have suggested that the initial infiltration of the hematogenous cells may be due to the secretion of cytokines and chemokines in the injured CNS. In order to elucidate which chemotactic factors may be expressed following traumatic spinal cord contusion, the presence of mRNA for a number of cytokines, chemokines and growth factors was examined in contused rat spinal cord by reverse transcriptase-polymerase chain reaction and immunohistochemistry. Spinal injury was accompanied by an increase in glial fibrillary acidic protein mRNA suggesting astrocyte activation and astrogliosis. TNFalpha message levels were upregulated as early as 1 h post injury and returned to baseline levels by 3 days post injury (DPI). By immunocytochemistry, staining for TNFalpha increased at 1 and 3 dpi and was predominantly diffuse in the necrotic tissue. The chemokines IP-10, MCP-1, and MIP-1alpha were also detected in the injured spinal cord. mRNA levels of IP-10 peaked around 6 h post injury and were upregulated up to 7 dpi. MCP-1 mRNA was detected at 1 h post injury and its levels returned to baseline by 14 dpi. An increase in MCP-1 staining was observed from 1 to 7 dpi. The staining was also diffuse in the necrotic tissue and also localized to cells near the site of injury. The presence of aFGF and bFGF was also detected in the injured spinal cord. mRNA for aFGF was detected at 0 time, increased at 6 h post injury, peaked at 3 days, and remained elevated up to 21 days. bFGF mRNA was initially detected at 1 h post injury, increased between 6 h and 3 days, declined thereafter and returned to baseline levels by 21 days.

Animals↗
PubMed2000

[Blunt chest trauma with severe pulmonary contusion and traumatic myocardial infarction].

In the literature the incidence of cardiac involvement in blunt chest trauma varies considerably. This reflects the diagnostic problems encountered in polytraumatised patients. We report the case of an 18 year old man who suffered bilateral pulmonary contusion and traumatic myocardial infarction following a motorbike accident. The myocardial infarct was diagnosed by means of ECG, cardiac enzymes and echocardiography. When the diagnosis was made the time for successful interventional treatment had lapsed. A coronary angiography was performed after stabilisation which revealed a proximal dilatation of the left anterior descending artery. Left ventricular function was severely impaired (ejection fraction 26%). Due to the pulmonary contusion respiratory support was required for 14 days. The course was further complicated by left ventricular failure with low output.

Accidents, Traffic↗
PubMed2001

[Conjunctival cyst: subconjunctival luxation of the lens following ocular contusion - a case report].

PATIENT: Presentation of a 75-year-old female with subconjunctival lens luxation, that was initially misdiagnosed as conjunctival cyst. Initial examination had been difficult due to vascularized stromal corneal scars and a large hyphema. The ocular history revealed an ocular contusion 11 months ago. Aphakia with subconjunctival lens luxation, iris incarceration, iridodialysis and covered scleral rupture were diagnosed by inspection, palpation, slit-lamp biomicroscopy, gonioscopy and ultrasound biomicroscopy. The lens and incarcerated iris tissue were removed, the scleral wound was sutured and a penetrating keratoplasty was performed in combination with anterior vitrectomy and implantation of a transclerally sutured posterior chamber lens. The histologic investigation of the subconjunctival tissue showed the complete lens with intact lens capsule and surrounding subconjunctival connective tissue. CONCLUSION: Hyphemas following ocular contusion are frequent findings. A large hyphema may masquerade alterations of other ocular structures. The differential diagnosis of posttraumatic prominent conjunctival "tumors" should include subconjunctival luxation of the lens.

Aged↗
PubMed2004

Treatment of muscle injuries by local administration of autologous conditioned serum: animal experiments using a muscle contusion model.

Muscle contusions represent a major part of sports injuries. The suggested treatments are generally sufficient to support muscle healing, but require a relatively long period of time. Given that autologous blood products are safe treatments, we have used a technique which stimulates the release of certain growth factors in the autologous conditioned serum (ACS). Those growth factors are known to improve the proliferative activity of myogenic precursor cells. Mice were subjected to an experimental contusion injury to their gastrocnemius muscle; one group received local injections of ACS at 2 hrs, 24 hrs, and 48 hrs after injury, a control group received saline injections. The histology results showed that satellite cell activation at 30/48 hrs post injury was accelerated and the diameter of the regenerating myofibers was increased compared to the controls within the first week after injury. ELISA results on the ACS have shown that the elevations in FGF-2 (460 %) and TGF-beta1 (82 %) could be partly responsible for the accelerating effects on regeneration due to proliferative and chemotactic properties. We conclude that ACS injection is a promising approach to reduce the time of recovery from muscle injury. In terms of clinical targets, this new approach could be used in the treatment of sports injuries and may also be interesting in postoperative situations.

Animals↗
PubMed2001

Reduction of pathological and behavioral deficits following spinal cord contusion injury with the selective cyclooxygenase-2 inhibitor NS-398.

Spinal cord injury (SCI) results in loss of locomotor function and development of abnormal chronic pain syndromes (mechanical allodynia, thermal hyperalgesia). Following injury, secondary mechanisms including release of excitatory amino acids, inflammation and lipid peroxidation damage neural cells through release of cytotoxic free radicals. We hypothesized that selective inhibition of cyclooxygenase-2 (COX-2), an inducible inflammatory mediator, would decrease tissue damage and subsequently reduce locomotor deficits and development of chronic central pain syndromes after injury. Fifteen minutes prior to receiving T13 spinal segment spinal cord contusion injury, 200-225-g male Sprague-Dawley rats received either vehicle (0.5 ml 1:1 v/v DMSO/saline, i.p., n = 20) or the selective COX-2 inhibitor NS-398 (5 mg/kg in DMSO/saline v/v, i.p., n = 20). Locomotor function via the BBB scale, and nociceptive behaviors measured by paw withdrawals to von Frey filaments and radiant heat stimuli were tested for 4 weeks postinjury. Histological examination and volumetric analysis of spinal cord tissue were performed concomitantly. Spinally contused animals receiving NS-398 demonstrated significantly (p < 0.05) reduced locomotor alteration and reductions in both fore- and hindlimb mechanical allodynia and thermal hyperalgesia when compared to vehicle controls. Histological examination of spinal segments at the lesion segment demonstrated reduced lesion extent and increased viable tissue when compared to vehicle controls. Prostaglandin E2 levels were significantly lowered in NS-398-treated but not vehicle-treated animals 12 h after injury. These results support the role of COX-2 in reducing pathological and behavioral deficits after spinal cord injury.

Animals↗
PubMed1988

Spinal cord contusion in the rat: somatosensory evoked potentials as a function of graded injury.

A weight-drop technique was used to produce mild, moderate, or severe spinal cord contusive injury in rats. At 4 weeks after injury, somatosensory evoked potentials (SEPs) were recorded with silver ball electrodes placed over the somatosensory cortex of anesthetized rats to measure the response to sciatic nerve stimulation. Both SEP area and amplitude were measured and were highly correlated with each other. Both indices of the SEP correlated inversely with the height of the weight drop and directly with the degree of residual function assessed at 4 weeks after injury. Measures of residual function consisted of a motor score, inclined plane test, and a combined behavioral score based on several neurologic functions. No correlation between latency of the SEP with degrees of contusive injury was observed. The data indicate that the SEP can be used as one criterion in the assessment of the severity of a lesion in a rat model of a graded spinal cord injury.

Animals↗
PubMed1993

Differential expression of MHC class II antigen in the contused rat spinal cord.

Following contusion injury to the dorsal surface of thoracic rat spinal cord, major histocompatibility complex (MHC) class II (Ia) antigen expression by microglia was evaluated throughout the developing lesion. Past investigations of various central nervous system (CNS) lesions have examined short-term or acute sequelae of post-traumatic Ia expression. This report demonstrates that in animals allowed to recover for 18 (sub-chronic) and 45 (chronic) days post-injury, MHC class II antigen is expressed differently at rostral and caudal extents of the lesion as compared with the lesion's epicenter. Following contusion injury to the thoracic spinal cord, sub-chronically injured animals demonstrated Ia-positive microglial staining throughout the white matter rostral and caudal to the epicenter of the lesion, whereas Ia-positive microglia and/or perivascular cells are localized within the gray matter adjacent to it. MHC class II immunoreactivity is down-regulated on microglia at chronic survival times but clusters of Ia-positive macrophages are prominent in regions of maximal degeneration at the epicenter of the lesion. Our findings support the theory that two distinct populations of macrophages participate in resolving traumatic injury. One population is the parenchymal CNS microglia and the other is presumably exudate macrophages derived from the blood. Furthermore, the immunocompetence of these cells as measured by MHC expression may be differentially regulated. This hypothesis is based on differences in Ia-positive staining observed between microglia and macrophages over time concomitant with differences in the spatial distribution of these cell types.

Animals↗
PubMed1997

Effects of mild hypothermia on nitric oxide synthesis following contusion trauma in the rat.

The exact mechanism of hypothermic cerebroprotection after traumatic brain injury (TBI) is not fully understood. The present study was conducted to investigate the effects of mild hypothermia on trauma-induced synthesis of nitric oxide (NO), which has been implicated in the pathogenesis of ischemic brain damage associated with glutamate neurotoxicity. Cerebral contusion was created in the rat parietal cortex by a weight-drop method, and extracellular concentrations of the NO end products nitrite and nitrate were measured using in vivo brain microdialysis and capillary electrophoresis under normothermic (37 degrees C) and mild hypothermic (32 degrees C) conditions. In normothermic animals, the level of NO end products increased markedly 10 min after contusion, reaching a maximum level at 20 min. In the hypothermic rats, such increases were absent. Although it is unknown whether endothelial NO synthase, neuronal NO synthase, or both caused the elevation of the NO end products seen in the normothermic animals, the present results indicate that inhibition of NO synthesis may play a part in hypothermic cerebroprotection following TBI.

Animals↗
PubMed1997

Quantitative analysis of acute axonal pathology in experimental spinal cord contusion.

The major sensorimotor deficits that result from traumatic spinal cord injury (SCI) are due to loss of axons in ascending and descending pathways of the white matter (WM). Experimental treatments administered after a standardized SCI can reduce WM loss and long-term functional deficits. Thus, a significant proportion of WM loss occurs secondary to the mechanical injury and may be a target for therapeutic intervention. Presently, we know little of how and when secondary injury mechanisms operate in the WM after SCI. We therefore used a standardized rat model of clinically relevant contusion injury to examine axonal pathology over the first 24 h by light and electron microscopy. Based on qualitative evaluation of tissue at 15 min, 4 h, and 24 h after a "mild" SCI produced with a weight-drop device (10 g x 2.5 cm), we selected areas from the ventromedial WM at the lesion epicenter for quantitative analyses. We compared axon number and the proportion of axons with various axoplasmic and myelin abnormalities over time after SCI, as well as the effect of axon size on degree of pathology and loss. We found by 4 h postinjury (pi) axonal pathology was more severe than at 15 min and that a significant loss of large diameter axons had occurred; no significant additional loss of axons was seen by 24 h pi. When we compared axonal pathology after a more severe contusion (10 g x 17.5 cm), we found a greater loss of axons at 4 h. In addition, a higher proportion of the remaining axons demonstrated pathological alterations. We developed a semi-quantitative Axonal Injury Index (AII) as an overall measure of axonal pathology that was sensitive to the effects of injury severity at 4 h pi. The AII has greater statistical power than our individual measures of axonal pathology. Our results suggest that it may be possible to use the AII at 4 h pi to assess effects of potential therapeutic agents on acute axonal pathology after SCI.

Animals↗
PubMed1998

Dissociable long-term cognitive deficits after frontal versus sensorimotor cortical contusions.

Cognitive deficits are the most enduring and disabling sequelae of human traumatic brain injury (TBI), but quantifying the magnitude, duration, and pattern of cognitive deficits produced by different types of TBI has received little emphasis in preclinical animal models. The objective of the present study was to use a battery of behavioral tests to determine if different impact sites produce different patterns of behavioral deficits and to determine how long behavioral deficits can be detected after TBI. Prior to surgery, rats were trained to criteria on delayed nonmatching to position, radial arm maze, and rotarod tasks. Rats received sham surgery (controls), midline frontal contusions (frontal TBI, 2.25 m/sec impact), or unilateral sensorimotor cortex contusions (lateral TBI, 3.22 m/sec impact) at 12 months of age and were tested throughout the next 12 months. Cognitive deficits were more robust and more enduring than sensorimotor deficits for both lateral TBI and frontal TBI groups. Lateral TBI rats exhibited transient deficits in the forelimb placing and in the rotarod test of motor/ambulatory function, but cognitive deficits were apparent throughout the 12-month postsurgery period on tests of spatial learning and memory including: (1)reacquisition of a working memory version of the radial arm maze 6-7 months post-TBI, (2) performance in water maze probe trials 8 months post-TBI, and (3) repeated acquisition of the Morris water maze 8 and 11 months post-TBI. Frontal TBI rats exhibited a different pattern of deficits, with the most robust deficits in tests of attention/orientation such as: (1) the delayed nonmatching to position task (even with no delays) 1-11 weeks post-TBI, (2) the repeated acquisition version of the water maze--especially on the first "information" trial 8 months post-TBI, (3) a test of sensorimotor neglect or inattention 8.5 months post-TBI, and (4) a DRL20 test of timing and/or sustained attention 11 months after surgery. These results suggest that long-term behavioral deficits can be detected in rodent models of TBI, that cognitive deficits seem to be more robust than sensorimotor deficits, and that different TBI impact sites produce dissociable patterns of cognitive deficits in rats.

Animals↗
PubMed1998

Assessment of lower urinary tract functional deficit in rats with contusive spinal cord injury.

Traumatic spinal cord injury (SCI) produces lower urinary tract (LUT) dysfunction that has been studied in surgical transection models. Our aim was to assess LUT functional deficit in a clinically relevant model of incomplete SCI to investigate how partial preservation of supraspinal connections might affect LUT dysfunction. Standardized weight-drop contusion (10 g x 2.5 cm) or complete transection, was produced at T8 in female Sprague-Dawley rats. Behavioral tests were used to assess hind limb sensorimotor function at Day 1 after surgery and weekly thereafter. The urometric experiments were conducted on groups (n = 7) of uninjured rats and on injured rats during Weeks 1 and 2 after SCI (before and after spontaneous voiding was established) as well as Week 2 after a complete transection (n = 3). Under anesthesia, the bladder was continuously perfused with saline. Changes in bladder pressure and external urethral sphincter (EUS) electrical activity were monitored. The bladder was then dissected and weighed and both the bladder and spinal cord were fixed for pathoanatomical analyses. Our results indicate that several aspects of LUT dysfunction after contusive SCI were similar to transection, e.g., reduction of voiding efficiency (approximately 5% of normal value), decrease in inter-contraction interval (47%), increase in bladder capacity (8-fold), and weight (4.6-fold). One aspect appeared different from transection--partial recovery from acute bladder/sphincter dyssynergia. Because the coordination of bladder and EUS function is mediated by brainstem pathways, partial recovery of synergy after SCI was likely due to sparing of some relevant bulbospinal projections as was confirmed by retrograde transneuronal viral tracing.

Animals↗
PubMed1999

Functional recovery after central infusion of alpha-melanocyte-stimulating hormone in rats with spinal cord contusion injury.

Melanocortins, peptides related to alpha-melanocortin-stimulating hormone (alpha MSH) and adrenocorticotropic hormone (ACTH), are known to improve axonal regeneration following peripheral nerve injury and stimulate neurite outgrowth from central nervous system (CNS) neurons both in vitro and in vivo. The neurite outgrowth promoting capacity of alpha MSH has prompted us to investigate the effects of intrathecal application of alpha MSH on functional and electrophysiological recovery in a well-characterized model of spinal cord contusion injury. Different doses of alpha MSH were applied via osmotic minipumps into the cisterna magna for 10 days, thereby delivering the peptide directly into the CNS. Functional recovery was monitored during 8 postoperative weeks by means of the Basso, Beattie, and Bresnahan locomotor rating scale, and the thoracolumbar height test. At the end of the study, electrophysiological analysis of rubrospinal motor evoked potentials as performed. Our data showed that application of 3.75 micrograms/kg/h alpha MSH resulted in a marked functional recovery, accompanied by a decrease in the latency of the rMEP. This study demonstrates that intrathecal application of alpha MSH results in functional recovery after spinal cord contusion injury. These findings may initiate new treatment strategies and/or the use of melanocortins in human spinal cord injury.

Analysis of Variance↗
PubMed2000

Rodent model of chronic central pain after spinal cord contusion injury and effects of gabapentin.

Spinal cord injury (SCI) often results in abnormal pain syndromes in patients. We present a recently developed SCI mammalian model of chronic central pain in which the spinal cord is contused at T8 using the NYU impactor device (10-g rod, 2.0-mm diameter, 12.5-mm drop height), an injury which is characterized behaviorally as moderate. Recovery of locomotor function was assessed with an open field test and scored using the open field test scale (BBB scale). Somatosensory tests of paw withdrawal responses accompanied by supraspinal responses to both mechanical punctate (von Frey hairs) and nonpunctate (4 mm diameter blunt probe) as well as thermal (radiant heat) peripheral stimuli were performed. Comparisons at the level of the individual animal between precontusion and postcontusion responses indicated significant increases in reactions to low threshold punctate mechanical stimuli, non-punctate stimuli and thermal stimuli (p < 0.05). To demonstrate the validity of this model as a central pain model, gabapentin, an agent used clinically for central pain, was given i.p. at 10 or 30 mg/kg. Gabapentin treatment significantly and reversibly changed the responses, consistent with the attenuation of the abnormal sensory behavior, and the attenuated responses lasted for the duration of the drug effect (up to 6 h). These results support the use of the spinal contusion model in the study of chronic central pain after SCI.

Acetates↗
PubMed1974

Cardiac trauma: Clinical and experimental correlations of myocardial contusion.

Clinical and experimental observations in myocardial contusion have been correlated. Cardiac arrhythmia is always an important consequence and may be fatal. Reduction in cardiac output often accompanies significant cardiac injury. The coronary arterial circulation is not interrupted and is generally enhanced to the area of injury. Healing of the injury under these circulatory conditions may result in patchy scarring and peculiar adynamic areas of myocardium. Early diagnosis of myocardial contusion may be aided using radionuclide imaging with (99m)Tc-Sn-polyphosphate.

Adult↗
PubMed1984

Increased renal parenchymal accumulation of Tc-99m HDP in kidney contusion.

Unilateral focal areas of intense, increased renal uptake of Tc-99m oxidronate sodium (technetium-99m HDP) were incidentally detected in the bone scan of a female patient who subsequently gave a history of recent trauma to her flank. Increased renal parenchymal uptake of Tc-99m HDP in this patient was thought to be due to kidney contusion. The case is interesting in itself and for its possible implications regarding the use of radio-labeled phosphate compounds for detection of renal contusion.

Adult↗
PubMed1997

Resuscitation of pulmonary contusion: effects of a red cell substitute.

OBJECTIVE: To determine the impact of a vasoactive red cell substitute, diaspirin cross-linked hemoglobin, on respiratory derangements after traumatic lung injury. DESIGN: Randomized, controlled animal experiment. SETTING: Large-animal laboratory. SUBJECTS: Mechanically ventilated, anesthetized young Yorkshire male swine (15 to 20 kg). INTERVENTIONS: Pigs (n = 6/group) received two pneumatic blasts to the right thoracic cage at baseline, were hemorrhaged 30 mL/kg from t = 0 to 20 mins, resuscitated with 0.9% saline (group 1, 90 mL/ kg) or diaspirin cross-linked hemoglobin (group 2, 15 mL/kg) from t = 20 to 40 mins, and then observed to t = 240 mins. MEASUREMENTS AND MAIN RESULTS: Serial pulmonary and systemic hemodynamic measurements, total thoracic compliance assessment, spiral three-dimensional computed tomography scan, and lung weights (n = 3/group) were used to assess lesion size and lung water. Mean arterial pressure was restored in both animal groups. Mean pulmonary arterial pressure was significantly higher after resuscitation in animals receiving the red cell substitute. Oxygenation worsened mildly in both groups. Compliance diminished in both groups but was significantly worse at the end of the experiment in animals infused with diaspirin cross-linked hemoglobin. Right lung weights and right thoracic computed tomography scan volume were higher with diaspirin cross-linked hemoglobin than with saline. CONCLUSIONS: After pulmonary contusion, resuscitation with diaspirin cross-linked hemoglobin led to pulmonary hypertension, greater pulmonary contusion lesion size, and stiffer lungs in this porcine model.

Animals↗