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[Experimental animal studies on lung contusion].

Isolating lung contusions were represented by means of animal experiments in rats. The mechanism of the trauma was a bounce against the thorax wall with a steel cylinder. Macroscopic pulmonary alterations, lung weights, the frequency of secondary injuries as well as the mortality rate are the parameters of the lesion. The lung alterations shows communities with human lung contusions. The model is suitable for the specification of histological and morphological alterations and for the pathogenesis of lung contusions as well as for the quest of diagnostic parameters. The intensity of the lung contusion is limited by initial rupture of vessels. To the test of clinical therapy and for the release of limited lung contusions there are required models with other mechanisms of trauma.

Animals↗

[Phase analysis of gated blood pool scintigraphy in traumatic myocardial contusion].

It is not easy to make a diagnosis of myocardial contusion following blunt chest trauma, because most patients have many other concurrent injuries with diverse symptoms. The usefulness of phase analysis of gated blood pool scintigraphy (GBPS) for myocardial contusion following blunt chest trauma was evaluated. Thirty-eight patients who had been strongly suspected of having myocardial contusion from clinical symptoms and electrocardiograms underwent phase analysis of GBPS. The results of phase analysis were compared with those of two-dimensional echocardiography (2-D Echo) and CPK-MB fraction measurement in all patients, with those of 201TlCl myocardial scintigraphy in 35 patients and with those of 99mTc-pyrophosphate scintigraphy in 10 patients. In 29 patients (76.3%), the results of phase analysis matched those of 2-D Echo. Two patients (5.3%) who were judged as positive by 2-D Echo and as negative by phase analysis had only rupture of the chordae. Only one of two other patients who were judged as negative by 2-D Echo and as positive by phase analysis was judged as positive by 201TlCl myocardial scintigraphy. The results of both 2-D Echo and phase analysis were not well correlated with those of CPK-MB fraction measurement and 99mTc pyrophosphate scintigraphy. It is concluded that phase analysis of GBPS, as well as 2-D Echo, is useful for diagnosing myocardial contusion, and that phase analysis is most useful for diagnosing myocardial contusion in patients who cannot be examined by 2-D Echo because of the presence of pneumothorax and/or subcutaneous emphysema in the anterior chest wall.

Adolescent↗

Outcome of isolated pulmonary contusion in blunt trauma patients.

To determine outcome in young, healthy blunt trauma patients with isolated pulmonary contusion, and to identify factors associated with poor outcome, we reviewed 6012 consecutive adult (aged 16-49) blunt trauma admissions. Ninety-four (7.9%) presented with an isolated pulmonary contusion defined by chest radiograph and Injury Severity Score < 25; they compromise the study group. Poor outcome was defined as death, prolonged hospitalization (> 7 days), or a severe complication (pneumonia, empyema, atelectasis requiring bronchoscopy, or bronchopleural fistula). None of the 94 study patients died. Admission chest radiograph demonstrated no contusion in 34 patients (36%). Fifteen patients (16%) required intubation, but 13 were extubated within 48 hours. Forty-one patients (44%) required insertion of a chest tube, and 20 patients (21%) had a PaO2/FiO2 ratio of < 250 on admission. Post-injury atelectasis (n = 17), pneumothorax (n = 17), effusion (n = 8), pneumonia (n = 2), empyema (n = 1), and Staphylococcal bacteremia (n = 1) complicated hospitalizations. The following clinical factors were identified as predisposing to poor outcome by univariate analysis: 1) Pulmonary contusion on admission chest radiograph (P = 0.035); 2) Three or more rib fractures (P = 0.002); 3) chest tube insertion (P = 0.010) and drainage (P = 0.020); and 4) hypoxia on admission (PO2 < 70 torr [P = .021], PaO2/FiO2 < 250 [P < 0.001]). Only PaO2/FiO2 < 250 on admission was an independent predictor of poor outcome in a multivariate analysis (P = 0.040). Our conclusion was that isolated pulmonary contusion in young, healthy patients is not associated with mortality.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Resuscitation of pulmonary contusion: hypertonic saline is not beneficial.

We postulated that hypertonic solutions could minimize the accumulation of lung water and subsequent respiratory derangements that occur after pulmonary contusion. Anesthetized pigs underwent contusion of the right chest at baseline and then were hemorrhaged (30 cc/kg) over 20 min. They were resuscitated with either 7.5% NaCl (4 cc/kg) or .9% saline (90 cc/kg) for 20 min and observed for 4 h. Gravimetric lung weights and spiral computed tomography scans were used to quantitate lung water. The hemodynamic response to contusion and hemorrhage was similar in both resuscitation groups. Arterial oxygen tension was not significantly altered by the method of resuscitation and remained close to baseline values for the entirety of the experiment. Static compliance measurements were significantly decreased from baseline in both groups following pulmonary contusion. There were no differences in wet to dry lung weights or computed tomography scan injury volume between groups. We conclude that small volume hypertonic saline resuscitation does not reduce the magnitude of lung injury or provide substantial physiologic benefit over isotonic solutions following pulmonary contusion.

Animals↗

Chemokine antagonist infusion promotes axonal sparing after spinal cord contusion injury in rat.

Spinal cord injury produced by mechanical contusion causes the onset of acute and chronic degradative events. These include blood brain barrier disruption, edema, demyelination, axonal damage and neuronal cell death. Posttraumatic inflammation after spinal cord injury has been implicated in the secondary injury that ultimately leads to neurologic dysfunction. Studies after spinal cord contusion have shown expression of several chemokines early after injury and suggested a role for them in the ordered recruitment of inflammatory cells at the lesion site (McTigue et al. [1998] J. Neurosci. Res. 53:368-376; Lee et al., [2000] Neurochem Int). We have demonstrated previously that infusion of the broad-spectrum chemokine receptor antagonist (vMIPII) in the contused spinal cord initially attenuates leukocyte infiltration, suppresses' gliotic reaction and reduces neuronal damage after injury. These changes are accompanied by increased expression of bcl-2, the endogenous apoptosis inhibitor, and reduced neuronal apoptosis (Ghirnikar et al. [2000] J. Neurosci. Res. 59:63-73). We demonstrate that 2 and 4 weeks of vMIPII infusion in the contusion-injured spinal cord also results in decreased hematogenous infiltration and is accompanied by reduced axonal degeneration in the gray matter. Luxol fast blue and MBP immunoreactivity indicated reduced myelin breakdown in the dorsal and ventral funiculi. Increased neuronal survival in the ventral horns of vMIPII infused cords was seen along with increased bcl-2 staining in them. Immunohistochemical identification of fiber phenotypes showed increased presence of calcitonin gene related peptide, choline acetyl transferase and tyrosine hydroxylase positive fibers as well as increased GAP43 staining in treated cords. These results suggest that sustained reduction in posttraumatic cellular infiltration is beneficial for tissue survival. A preliminary report of this study has been published (Eng et al. [2000] J. Neurochem. 74(Suppl):S67B). In contrast to vMIPII, infusion of MCP-1 (9-76), a N-terminal analog of the MCP-1 chemokine showed only a modest reduction in cellular infiltration at 14 and 21 dpi without significant tissue survival after spinal cord contusion injury. Comparing data on tissue survival obtained with vMIPII and MCP-1 (9-76) further validate the importance of the use of broad-spectrum antagonists in the treatment of spinal cord injury. Controlling the inflammatory reaction and providing a growth permissive environment would enhance regeneration and ultimately lead to neurological recovery after spinal cord injury. J. Neurosci. Res. 64:582-589, 2001. Published 2001 Wiley-Liss, Inc.

Amino Acid Sequence↗

Degeneration and sprouting of identified descending supraspinal axons after contusive spinal cord injury in the rat.

Contusive spinal cord injury (SCI) results in the formation of a chronic lesion cavity surrounded by a rim of spared fibers. Tissue bridges containing axons extend from the spared rim into the cavity dividing it into chambers. Whether descending axons can grow into these trabeculae or whether fibers within the trabeculae are spared fibers remains unclear. The purposes of the present study were (1) to describe the initial axonal response to contusion injury in an identified axonal population, (2) to determine whether and when sprouts grow in the face of the expanding contusion cavity, and (3) in the long term, to see whether any of these sprouts might contribute to the axonal bundles that have been seen within the chronic contusion lesion cavity. The design of the experiment also allowed us to further characterize the development of the lesion cavity after injury. The corticospinal tract (CST) underwent extensive dieback after contusive SCI, with retraction bulbs present from 1 day to 8 months postinjury. CST sprouting occurred between 3 weeks and 3 months, with penetration of CST axons into the lesion matrix occurring over an even longer time course. Collateralization and penetration of reticulospinal fibers were observed at 3 months and were more extensive at later time points. This suggests that these two descending systems show a delayed regenerative response and do extend axons into the lesion cavity and that the endogenous repair can continue for a very long time after SCI.

Acute Disease↗

The antioxidant effect of N-acethylcysteine on experimental contusion in rats.

N-acethylcysteine (NAC) is known to have direct and indirect antioxidant abilities. We investigated the potential protective effect of NAC on ICP, brain edema and contusion volume after Controlled Cortical Impact (CCI) injury. A moderate CCI injury was induced on the left hemisphere in 48 Sprague Dawley rats. The animals were treated with intraperitoneal injection of NAC (163 mg/kg/KG) or physiological saline. Measurements of intracranial pressure (ICP) were performed and brains were removed at 24 hours. Gravimetric analysis of post-traumatic edema and morphometric measurements (TTC staining) of contusion volume were carried out in 24 animals, respectively. ICP measurements increased significantly over time with no significant differences between both groups. The relative difference in water content in NAC treated animals (1.45 +/- 0.1%) did not differ significantly versus placebo (1.47 +/- 0.2%). The contusion volume was diminished by 19% in the NAC group (53.52 +/- 5.3 mm3) versus placebo (66.28 +/- 4.7 mm3) without showing statistical significance. The antioxidant properties of NAC did not affect intracranial pressure or posttraumatic brain edema formation, although the moderate reduction of contusion volume might reveal beneficial effects on focal contusion.

Acetylcysteine↗

Gadolinium DTPA-enhanced magnetic resonance imaging of cerebral contusions.

The morphological characteristics of cerebral contusions in head trauma patients suggest that an increase in cerebrovascular permeability is responsible for the contusion edema which develops within 1-3 days posttrauma. In the present study, 10 patients with cerebral contusions (mean age, 38 years old; 8 males and 2 females) were examined by gadolinium (Gd)-DTPA enhanced magnetic resonance imaging (MRI) at 1-2 days after trauma. Gd-DTPA (0.3 mmol/kg) was infused intravenously over a period of 30 min. MRIs were taken before, and at 2 and 4 hours after initiation of the Gd-DTPA administration. It was found that contusion edema areas were frequently enhanced by Gd-DTPA at 2 hours. The enhancement diminished at 4 hours. These findings appear to be inconsistent with the results of previously reported similar studies in which enhancement was detected at 6-9 days posttrauma but not during the period earlier than 6 days. This discrepancy may be attributable to the presence of a high blood concentration of Gd-DTPA for a longer period of time and a delay in the time at which MRIs were taken in the present study. The present data indicate that an increased cerebrovascular permeability occurs at as early as 1-2 days posttrauma, and suggest that contusion edema which progresses during the initial 1-3 days may be at least partially vasogenic in nature.

Adolescent↗

Regional cerebral blood flow in the pig after a localized cerebral contusion treated with barbiturates.

Regional cerebral blood flow determined with microsphere technique in anaesthetized pigs was measured before and after a localized cerebral contusion as well as after treatment with pentobarbital. No overall reduction in intracranial pressure or perfusion pressure was observed. Flow reduction due to pentobarbital was different in different regions with a high percentage change in the highly perfused basal structures and cortical grey matter except in the centre of the contusion where the reduction was half compared to the rest of cortical grey matter. Changes in white matter were less than in cortical grey matter but more pronounced than in the very high flow areas (choroid plexus and pineal gland). The accumulated change was greatest in the damaged region. Contralateral to the contusion, where a significant increase in flow was noticed after the contusion, there was a very low accumulated change in flow. In white subcortical matter underlying the contusion a similar low flow change was observed but this was not accompanied by as large an accumulated change as in grey cortical matter. At each fraction of injected pentobarbital a short-lasting increase in intracranial pressure and a reduction in mean arterial blood pressure was observed. The amplitude and the height of the intracranial pressure change was reduced during the pentobarbital injections.

Animals↗

Traumatic brain contusions: a clinical role for the kinin antagonist CP-0127.

Focal cerebral contusions can be dynamic and expansive, leading to delayed neurological deterioration. Due to the high mortality associated with such cerebral contusions, our standard practice had evolved into evacuating contusions in patients who had a deterioration in level of consciousness, lesions > 30 cc and CT suggestion of raised ICP. Experimental brain edema studies have implicated kinins in causing 2 degrees brain swelling. CP-0127 (Bradycor), a specific bradykinin antagonist, has been found to reduce cerebral edema in a cold lesion model in rats. In a randomized, single blind pilot study, a 7 day infusion of CP-0127 (3.0 micrograms/kg/min) was compared to placebo in patients with focal cerebral contusions presenting within 24-96 hours of closed head injury with an initial GCS 9-14. The ICP, GCS, and vital signs were monitored hourly. The total lesion burden (TLB) was measured on serial CT scans. There were no differences in age, baseline GCS, TLB, initial ICP, or laboratory findings between the two groups (n = 20). The mean (+/- s.d.) rise in peak ICP from baseline was greater in the placebo group than with CP-0127 (21.9 +/- 4.7 vs 9.5 +/- 2.0, P = 0.018). In addition, the mean reduction in GCS in the placebo group was significantly greater than in the CP-0127 group (4 +/- 1.0 vs 0.6 +/- 0.4, P = 0.002). Significantly raised ICP and clinically significant neurological deterioration occurred in 7/9 patients on placebo (77%) and only in 1 patient (9%; n = 11) on CP-0127, mandating surgery (P = 0.005). There were no adverse drug reactions, significant changes in vital signs or variations in the laboratory values. The cerebral perfusion pressure was adequately maintained in all patients irrespective of therapy. These preliminary results with CP-0127 provide supporting evidence that the kinin-kallikrein system could be involved in cerebral edema. In this study, treatment with CP-0127 appeared to alter the natural history of traumatic brain contusions by preventing the 2 degrees brain swelling. In addition, CP-0127 obviated the need for surgery in the majority of treated patients. CP-0127 could act on the cerebral vasculature to limit dys-autoregulation and brain swelling or on the blood brain barrier to reduce cerebral edema.

Adult↗

Responses to cortical injury: I. Methodology and local effects of contusions in the rat.

In order to develop some understanding of the evolution of cortical contusions, interdisciplinary studies including behavior, morphology and histochemistry were conducted at varying intervals after standardized injuries. A method for producing graded and reproducible focal cortical contusions in the rat is described. When these impact injuries are made in the "hindpaw cortical area,' specific trauma dose dependent behavioral deficits can be readily observed in the contralateral hindlimb. While most functional recovery occurs in the first two weeks after trauma, with severe contusions, deficits persist beyond 90 days. Morphologically these injuries progress from hemorrhages in white matter directly under contused cortex during the first hours after injury to the development of a necrotic cavity by 24 hours. The cavitation appears to expand over the subsequent two weeks and by 15 days is lined with fibroblast-like elements and macrophages. Intense acid phosphatase activity is seen on the borders of the area of necrosis. This lysosomal enzyme may participate in autolysis and development of focal cavitation following cortical contusion.

Acid Phosphatase↗

CT evidence of intracranial contusion and haematoma in relation to the presence, site and type of skull fracture.

The skull films and CT scans of 1383 patients with acute head injury transferred to a regional neurosurgical unit were reviewed. Of the 850 patients with a skull fracture, contusion and/or haematoma was found in 71%, compared with 46% of the 533 patients with no fracture. Thirty-nine per cent of patients had neither contusion nor haematoma, and 21% had neither skull fracture nor contusion/haematoma. Haematomas occurred more frequently in association with lateral and occipital fracture than with frontal fracture, but the incidence of contusion was similar for all fracture sites. Linear fractures were more often associated with extra- and subdural haematomas than were depressed fractures. Intracranial damage associated with depressed fractures was localized more frequently than with linear fractures. Frontal fractures were rarely associated with posterior damage alone, but with occipital fractures anterior contusion was more frequent than posterior. Damage associated with lateral fracture was solely contralateral in 26%. Skull fracture was present in 77% of patients with contusion, 87% of those with an extradural, 72% with a subdural, and 66% with an intracerebral haematoma (70% of all those with an intracranial haematoma).

Brain Concussion↗

Orbital-frontal delayed hemorrhagic contusions: clinical course and neurosurgical treatment protocol.

BACKGROUND: Delayed posttraumatic hemorrhage into the underlying contusion could cause significant elevation of intracranial pressure (ICP) and dramatic clinical and radiographic deterioration. The authors identified a subgroup of young patients with initial mild/moderate head injury, who presented with orbito-frontal and temporal tip minimal punctate contusions, which within 24 hours, expanded into dramatically larger noncoalesced hemorrhagic contusions. METHODS: Four consecutive patients within a 13-month period admitted to our institution with the above radiographic picture are presented and their clinical and treatment courses compared. RESULTS: After observing the relentless downhill course of two earlier patients treated for the control of ICP, our treatment protocol changed to early prophylactic intubation and moderate hyperventilation, insertion of an intraventricular catheter for ICP monitoring, hyperosmolar therapy with mannitol, sedation, chemical paralytics, and eventually pentobarbital for control of increased ICP. These interventions were mostly taken before the radiographic evidence of contusion blossoming and dramatic clinical deterioration. These two subsequent patients had a prolonged course of intubation and ICP problems requiring tracheostomy placement. The clinical outcome was excellent, however, with both patients decanulated from the tracheostomy within 6 weeks, and both returned to relatively normal premorbid functions. CONCLUSION: Although the series consists only of four consecutive patients with similar radiographic appearances, the authors advocate ultra-early aggressive medical treatment for this subgroup of patients with orbito-frontal contusion, prior to dramatic clinical and radiographic deterioration, as the outcome difference could be great.

Adult↗

Cathepsin B mRNA and protein expression following contusion spinal cord injury in rats.

We provide the first data that cathepsin B (Cath B), a lysosomal cysteine protease, is up-regulated following contusion-spinal cord injury (SCI). Following T12 laminectomy and moderate contusion, Cath B mRNA and protein expression profiles were examined from 2 to 168 h post-injury in rats using real-time PCR and immunoblots, respectively. Contusion injury significantly increased [mRNA]Cath B in the injury site and adjacent segments over sham injury levels. While the largest [mRNA]Cath B induction (20-fold over naive) was seen in the injury site, the caudal segment routinely yielded [mRNA]Cath B levels greater than 10-fold over naive. Interestingly, sham injury animals also experienced mRNA induction at several time points at the injury site and in segments rostral and caudal to the injury site. Contusion injury also significantly elevated levels of Cath B proenzyme protein (37 kDa) over sham injury in the injury site (48, 72 and 168 h post-injury). Furthermore, significant protein increases of single and double chain Cath B (both active forms) occurred at the injury site at 72 and 168 h post-injury. Similar significant increases in Cath B protein levels were seen in areas adjacent to the injury site. The induction of Cath B mRNA and protein expression following contusion injury is previously undescribed and suggests that Cath B may potentially be involved in the secondary injury cascade, perhaps for as long as 1 week post-injury.

Animals↗

[Computerized tomographic findings in brain contusions (author's transl)].

Over a 1 1/2 year period computerized tomographical examinations were performed on 104 patients suffering from brain concussions. The evaluation of findings resulted in the following classification: Type 1: severe generalized brain oedema without visible contusional foci, Type IIa: typical contusion with solitary or multiple contusional foci, Type IIb: typical contusion with severe, locally pronounced oedema, Type IIIa: contusion with flat subdural contusional bleeding, Type IIIb: contusion with minor intracerebral contusional bleeding, Type IIIc: contusion with intraventricular bleeding. Space-occupying haemorrhages were excluded. The comparison of computerized tomographic findings with the clinical course justifies such a classification. There are significant correlation between CT findings and the clinical picture, especially with the degree of clouding of consciousness as well as with further prognosis.

Brain↗

Nonhemorrhagic cord contusion after percutaneous fiducial placement: case report and surgical recommendations.

STUDY DESIGN: Single case report and extensive literature review. OBJECTIVES: To present the first such report of cervical cord contusion after the percutaneous placement of gold-seed fiducials. The pathomechanics and surgical recommendations are reviewed. BACKGROUND: Spinal cord injuries are well documented in the medical literature. These injuries range from cord contusion to transection and result primarily from trauma. A single case report of a patient who was found to have a nonhemorrhagic cervical spinal cord contusion after percutaneous fiducial implantation is presented. METHODS: Single case report. RESULTS: The patient underwent percutaneous placement of fiducials for stereotactic radiosurgery for a nerve sheath tumor. Postoperatively she had primarily sensory complaints; no motor deficits were detected on neurological examination. Neuroimaging studies demonstrated nonhemorrhagic cervical cord contusion. She was treated conservatively and had complete resolution of her symptoms. CONCLUSIONS: The likely mechanism for the contusion was neck hyperextension during thrusting maneuvers during fiducial implantation. This is yet another report of normal intraoperative-evoked potentials with postoperative neurological sequelae. A dedicated team approach involving ancillary staff, anesthesiologists, and surgeons should be utilized to avert this potentially devastating complication.

Cervical Vertebrae↗

Effect of posttraumatic hyperglycemia on contusion volume and neutrophil accumulation after moderate fluid-percussion brain injury in rats.

The purpose of this study was to evaluate the effects of posttraumatic hyperglycemia on contusion volume and neutrophil accumulation following moderate traumatic brain injury (TBI) in rats. A parasagittal fluid-percussion (F-P) brain injury (1.8-2.1 atm) was induced in male Sprague-Dawley rats. Rats were then randomized into four trauma groups (n = 7/group) by the timing of dextrose injection (2.0 gm/kg/ip), which included (1) early (E) group: 5 min after TBI; (2) delayed (D) group: 4 h after TBI; (3) 24-h group: 24 h after TBI; or (4) control (C) group: no dextrose injection. A sham operated control group also received dextrose to document physiological parameters (n = 4). Rats were perfusion fixed 3 days following TBI, and the brains were processed for routine histopathological and immunocytochemical analysis. Contusion areas and volumes, as well as the frequency of myeloperoxidase immunoreactive polymorphonuclear leukocytes (PMNLs) were determined. Dextrose injections significantly increased blood glucose levels (p < 0.005) in all treated groups. Although acute hyperglycemia following TBI did not significantly affect total contusion volume, contusion area was significantly elevated in the early treatment group. In addition, early posttraumatic hyperglycemia enhanced neutrophil accumulation in the area of the cortical contusion (p < 0.005). In contrast, delayed induced hyperglycemia (i.e., 4 h, 24 h) did not significantly affect histopathological outcome or neutrophil accumulation. Taken together, these findings indicate that acute but not delayed hyperglycemia aggravates histopathological outcome and increased accumulation of PMNLs. Posttraumatic hyperglycemia in the acute phase may worsen traumatic outcome by enhancing secondary injury processes, including inflammation.

Animals↗

Combined demyelination plus Schwann cell transplantation therapy increases spread of cells and axonal regeneration following contusion injury.

Several cell populations have been shown to provide a permissive environment for axonal extension following transplantation to injury sites. The limited spread of transplanted cells from implantation sites in the mature CNS, and the superior substrate and trophic environment that they provide, likely contribute to the fact that few transplantation-based therapies have elicited axonal extension beyond the transplant. The aim of this study was to determine whether (1) regions of demyelination cranial and caudal to a spinal cord injury site would improve the spread of Schwann cells transplanted into the site of injury, and (2) whether this combination therapy was associated with improved anatomical regeneration. Three days following contusion injury, anti-galactocerebroside antibodies plus complement proteins were injected into the dorsal column cranial and caudal to the injury site, resulting in complete and well defined regions of demyelination that extended 8 mm either side of the injury site. One day later, naïve Schwann cells in suspension were injected into the contusion site. Transplanted Schwann cells homogeneously redistributed throughout the contusion site and the adjacent regions of demyelination cranial and caudal to the contusion site, providing a long-distance prospective path for repair that was free of myelin and contained transplanted cells. Animals that received demyelination plus transplantation therapy, but not untreated or single-treatment groups, exhibited robust axonal regeneration beyond the contusion site within the treated dorsal column. Axonal regeneration in these animals was not associated with an improvement in locomotor ability. These findings suggest that this combination therapy may overcome a central limitation of transplant strategies in which the permissive environment provided remains at the implantation site.

Animals↗