Timing of cortical contusion. Correlation between histomorphologic alterations and post-traumatic interval.
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The lesion was caused by a compression injury to the retina with a vitrectomy instrument in a rhesus monkey; the lesion was examined by electron microscopy 8 years later. The inner surface of the choroid was lined by a layer of cells with the characteristics of fibroblasts. The choriocapillaris was missing. Bruch's membrane was extremely thickened and showed numerous changes. In the center of the scar, the retinal pigment epithelium was discontinuous. The neuroretinal portion of the scar was composed of distorted and dislocated nerve cells, nerve fibers, and glial elements that were probably Müller cells. Towards the vitreous cavity, the surface of the scar contained numerous microvillous processes. A band of zonulae adherentes resembling the outer limiting membrane was seen immediately adjacent to the surface. No inner limiting membrane was seen in the entire scar area.
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The striated nephrogram following renal trauma is reported for the first time. Previously, the striated parenchymal pattern has been oted in obstruction and in a small number of cases of hypotension. Tamm-Horsfall proteinuria, and renal vein thrombosis.
The number of published cases of adolescents surviving thoracic aortic injuries with accompanying severe thoracic injuries is small. Only 20-30% of all these patients reach the trauma center alive. In the present case we demonstrate the diagnostic, operative and intensive care management in a 15-year-old girl. The exact interpretation of the AP thoracic X-ray in connection with a typical mechanism of injury led to the detection of a haemomediastinum. This is very important in the further development of diagnostics, because the conventional X-ray picture does not show significant signs in the case of an incomplete aortic rupture. Diagnostic hints have to be derived from the detection of the haemomediastinum. The girl was operated on under left heart bypass. Spinal ischaemia was absent after surgery, and renal failure also did not occur. The adjacent severe lung confusion healed under kinetic therapy with a kinetic treatment table without pulmonary complications.
OBJECTIVE: a) to describe a non-barotraumatic ventilatory setting for independent lung ventilation (ILV); b) to determine the utility of single lung end-tidal CO(2) (EtCO(2)) monitoring to evaluate the ventilation to perfusion (V/Q) matching in each lung during ILV and for ILV weaning. DESIGN: prospective study. SETTING: general intensive care unit in a university teaching hospital. PATIENTS: twelve patients with unilateral thoracic trauma needing ILV. INTERVENTIONS AND RESULTS: ILV was started with each lung ventilated with the same tidal volume (Vt): plateau airway pressure (Pplat) was 34.2+/-3.2 cmH2O in diseased lungs (DL) and 18.1+/-1.9 cmH2O in normal lungs (NL) ( P<0.01). Static compliance (Cst) was 9.9+/-1.1 ml/cmH(2)O in DL and 19.3+/-1.7 ml/cmH(2)O in NL ( P<0.01). EtCO2 was 22.5+/-2.2 mmHg in DL and 36.6+/-1.9 mmHg in NL ( P<0.01). PaO(2)/FiO(2) was at 151+/-20. PEEP was applied on the DL and each lung was ventilated with a Vt that developed Pplat < or =26 cmH2O. With this setting, Vt given to the NL was unchanged, whereas it was reduced in the DL (238+/-30 ml vs 350+/-31 ml; P<0.01). Cst and EtCO2 were still significantly lower in the DL ( P<0.01, respectively), while the PaO(2)/FiO(2) ratio remained unchanged. Vt was then progressively increased in the DL as Pplat decreased, but remained unchanged in the NL. ILV was discontinued when Vt, Cst and EtCO(2) were the same in each lung. PaO(2)/FiO(2) ratio had then increased to 295+/-18. CONCLUSIONS: a) during ILV, adequate oxygenation and a reduction in V/Q mismatch can be obtained by setting Vt and PEEP to keep Pplat below a safe threshold for barotrauma; b) measurement of single lung EtCO2 can be useful to evaluate progressive V/Q matching.
INTRODUCTION: Isolated trauma of the optic nerve usually occurs in association with blunt skull trauma involving fractures of the skull and optic canal, but rarely occurs from blunt ocular trauma. CASE REPORT: A 7-year old boy fell and struck his left eye against a toy antenna. The initial examination revealed a visual acuity of 0.2 and slight edema of the optic nerve head. Perimetry revealed a defect in the superior and nasal visual fields. CT and MRI scans of the orbit were normal. Nine months after the injury, vision had improved to 1.0. On examination, optic nerve atrophy had developed and perimetry continued to display a defect in the superior visual fields. DISCUSSION: The mechanism of optic nerve damage secondary to trauma can be classified as primary or secondary. Primary damage occurs as a result of external forces at the moment of trauma, e.g., rupture of nerve fibers or of capillary vessels. Secondary damage may not be present initially, but may occur later on and results from compromised blood supply to the optic nerve, e.g., following edema or angiospasm. In our patient, it is not clear whether the damage was primary or secondary. CONCLUSION: Damage to the optic nerve can be caused by blunt skull trauma and, rarely, also by blunt ocular trauma. This fact is of importance when considering legal and reimbursement issues.
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Several experimental brain oedema models are currently available, but most of them are very different from what happens in clinical practice. As it is simple and seems to replicate the range of injuries seen in man we decided to evaluate Marmarou's model of head injury in order to test physiopathogenic and therapeutic hypotheses. Three groups of Wistar rats weighting 360-400 gr, anaesthetized with sodium pentobarbitone and breathing spontaneously, without tracheal intubation, were studied. In the first group six animals were killed two hours after injury and the brain's water content compared with that of nine controls. In another group Evans blue (100 mg/kg) was injected one hour before trauma and dye's extraction ratio determined at various times after injury: five animals at 15 minutes, six at 30 minutes, five at 60 minutes and nine at 120 minutes. A total of twenty-eight animals served as controls. In the last group morphological studies with light and electron microscopy were performed in the traumatized brain tissue from rats killed 5 and 120 minutes after injury and in brain tissue from control rats. Results showed that Marmarou's brain trauma model induced perivascular brain oedema, already visible at the ultrastructural level 5 minutes after the injury. Endothelial cells themselves were "oedematiated", rich in pinocytotic vesicles and membrane blebs, and presented intact tight junctions. Two hours after trauma the perivascular oedema was more marked. At this time the brain water content was significantly higher than that in controls. Evans blue extraction ratio increased linearly with time, being significantly higher than in controls 120 minutes after injury. We conclude that Marmarou's model is a suitable model for the study of brain oedema induced by trauma, and that this oedema, assessed by three different methodologies, was statistically significant two hours after injury.
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Seventy-five patients with nonpenetrating chest injuries were evaluated with electrocardiography, cardiac enzyme determination, 2-dimensional echocardiography and radionuclide ventriculography to document the incidence of cardiac abnormalities. Although the electrocardiograms showed ST-T wave changes in 25 patients (33%), sensitivity (47%) and specificity (79%) for echocardiographic and radionuclide abnormalities were poor. Cardiac enzymes were abnormal in 10 patients (13%), sensitivity for echocardiographic or radionuclide abnormalities, or both, was 29% and specificity 90%. Wall motion abnormalities were detected in 11 patients (18%) by radionuclide studies and in 3 patients (6%) by echocardiography. A pericardial effusion was present in 5 patients (10%). Two patients (4%) died of noncardiac causes; neither had wall motion abnormalities. This study documents the favorable outcome of patients with blunt chest injuries and does not suggest that echocardiography or radionuclide studies should be performed routinely on such patients.
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