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1/42. rupture mechanism of a thrombosed slow-growing giant aneurysm of the vertebral artery--case report.

    A 76-year-old male developed left hemiparesis in July 1991. The diagnosis was thrombosed giant vertebral artery aneurysm. He showed progressive symptoms and signs of brainstem compression, but refused surgery and was followed up without treatment. He died of rupture of the aneurysm and underwent autopsy in March 1995. Histological examination of the aneurysm revealed fresh clot in the aneurysmal lumen, old thrombus surrounding the aneurysmal lumen, and more recent hemorrhage between the old thrombus and the inner aneurysmal wall. The most important histological feature was the many clefts containing fresh blood clots in the old thrombus near the wall of the distal neck. These clefts were not lined with endothelial cells, and seemed to connect the lumen of the parent artery with the most peripheral fresh hemorrhage. However, the diameter of each of these clefts is apparently not large enough to transmit the blood pressure of the parent artery. Simple dissection of the aneurysmal wall by blood flow in the lumen through many clefts in the old thrombus of the distal neck may be involved in the growth and rupture of thrombosed giant aneurysms of the vertebral artery.
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2/42. Cerebral arterial gas embolism in air force ground maintenance crew--a report of two cases.

    Two cases of cerebral arterial gas embolism (CAGE) occurred after a decompression incident involving five maintenance crew during a cabin leakage system test of a Hercules C-130 aircraft. During the incident, the cabin pressure increased to 8 in Hg (203.2 mm Hg, 27 kPa) above atmospheric pressure causing intense pain in the ears of all the crew inside. The system was rapidly depressurized to ground level. After the incident, one of the crew reported chest discomfort and fatigue. The next morning, he developed a sensation of numbness in the left hand, with persistence of the earlier symptoms. A second crewmember, who only experienced earache and heaviness in the head after the incident, developed retrosternal chest discomfort, restlessness, fatigue and numbness in his left hand the next morning. Both were subsequently referred to a recompression facility 4 d after the incident. Examination by the diving Medical Officer on duty recorded left-sided hemianesthesia and Grade II middle ear barotrauma as the only abnormalities in both cases. Chest x-rays did not reveal any extra-alveolar gas. Diagnoses of Static Neurological decompression Illness were made and both patients recompressed on a RN 62 table. The first case recovered fully after two treatments, and the second case after one treatment. magnetic resonance imaging (MRI) of the brain and bubble contrast echocardiography performed on the first case 6 mo after the incident were reported to be normal. The second case was lost to follow-up. decompression illness (DCI) generally occurs in occupational groups such as compressed air workers, divers, aviators, and astronauts. This is believed to be the first report of DCI occurring among aircraft's ground maintenance crew.
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3/42. Cerebral air embolism and cerebral edema: one regimen of treatment.

    A case of cerebral air embolism responding immediately to compression to 6 atm is described. The patient, however, developed apparent cerebral edema while being decompressed. Subsequent recompression on oxygen was carried out twice daily at 60 ft (18 m, 2.8 ATA) for 60 min until the patient's symptoms had nearly cleared. While a number of other medications known to affect intracranial pressure were used, objective clinical improvement was noted only after hyperbaric oxygen. A question is raised of whether there is an association between the development of cerebral edema and the administration of intravenous 5% glucose in water.
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4/42. pneumothorax as a complication of recompression therapy for cerebral arterial gas embolism.

    The danger from pneumothorax in patients who undergo compression chamber treatment for cerebral arterial gas embolism (CAGE) following pulmonary barotrauma is frequently emphasized. Two cases of CAGE treated by recompression after submarine escape tank training (SETT) accidents are described. Both were complicated by bilateral pneumothoraces but the first case, treated on an air table, required thoracentesis in the chamber, whereas the second case, treated on an oxygen table, escaped the need for in-chamber thoracentesis despite large pneumothoraces. review of similar Royal Navy and united states Navy SETT accidents suggests that the danger from pneumothorax during recompression treatment of CAGE victims may be overstated. Modern management on oxygen-based therapeutic recompression tables may significantly reduce the risk. Thoracentesis while under pressure should be reserved for cases developing symptoms or signs of tension pneumothorax. Treatment options for these cases are discussed and a decision algorithm is proposed.
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5/42. Deep cerebral venous thrombosis in thalamo-ventricular hemorrhage of the term newborn.

    Unilateral thalamic bleeding with associated intraventricular hemorrhage is reported in three full-term neonates. The first presented within 48 hours from birth with early onset streptococcal meningitis, persistent pulmonary hypertension, tonic seizures and a tense fontanelle. The second presented 6 days after birth with irritability, opisthotonus, a tense fontanelle and tonic seizures. The third was admitted three days after birth with seizures and a tense fontanelle. In the latter two infants NMR and CT imaging documented thrombosed superficial and deep cerebral veins. The etiopathogenesis of intracranial venous thrombosis in the neonate is diverse: asphyxia, dehydration, polycythemia, sepsis-meningitis and difficult delivery are the main causes. In one of our patients jugular vein compression by the collar of a negative-pressure ventilation chamber probably initiated the intracranial events. More than half of the survivors sustain severe neurological impairment.
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6/42. Giant thrombus trapped in foramen ovale with pulmonary embolus and stroke.

    We describe the case of a young man who, while he was in coma because of a traffic accident, had first a pulmonary embolus and immediately afterwards had a systemic (cerebral) embolus. A transesophageal echocardiographic image revealed a giant thrombi trapped in foramen ovale protruding in right and left ventricles, diagnosing, thus, a paradoxical embolism. The relationship between patent foramen ovale and pulmonary embolism has been reported in some series. Elevated right-chamber pressure caused by pulmonary hypertension could favor the establishment of a right-to-left shunt, causing, in some cases, paradoxical embolisms. We review the clinical implications.
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7/42. Paradoxic embolism due to altered hemodynamic sequencing following transvenous pacing.

    A young patient, who experienced a cerebral embolic event 30 days after transvenous pacemaker lead placement, is reported. This patient had previously been paced with an epicardial lead without evidence of right to left intracardiac shunt. However, hemodynamic evaluation post-embolism demonstrated a marked temporal disparity of the pulmonary and systemic ventricles. This phasic divergence resulted in a brief reversal of right and left ventricular pressure ratios, and a paradoxic intracardiac shunt at a small ventricular septal defect. The potential for similar events in the presence of any defect of the atrial or ventricular septum mandates caution in the use of transvenous pacemaker leads in such patients.
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8/42. Transesophageal echocardiographic demonstration of distinct mechanisms for right to left shunting across a patent foramen ovale in the absence of pulmonary hypertension.

    The optimal visualization of the atrial septum and fossa ovalis by transesophageal echocardiography was utilized to demonstrate saline contrast transit across the atrial septum and to relate it to the motion of the flap valve (septum primum) of the fossa ovalis. In three cases, three distinct mechanisms of right to left interatrial shunting in the absence of right ventricular systolic hypertension were identified: 1) transient spontaneous reversal of the left to right atrial pressure differential with each cardiac cycle; 2) sustained elevation of right atrial pressure above left atrial pressure induced by respiratory maneuvers; and 3) aberrant flow redirection across the foramen ovale due to a large right atrial mass. Any of these three mechanisms may be operative during paradoxic embolism in the absence of elevation of right ventricular pressures.
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9/42. The neurological complications of cardiac transplantation.

    review of the neurological complications encountered in 83 patients who received cardiac homografts over a seven-year period leads to the following conclusions: (1) Neurological disorders are common in transplant recipients, occurring in over 50 per cent of patients. (2) infection was the single most frequent cause of the neurological dysfunction, being responsible for one-third of all CNS complications. (3) The infective organisms were typically those considered to be usually of low pathogenicity: fungi, viruses, protozoa and an uncommon bacterial strain. (4) Other clinical neurological syndromes were related to vascular lesions, often apparently from cerebral ischaemia or infarction occurring during the surgical procedure, metabolic encephalopathies, cerebral microglioma, acute psychotic episodes and back pain from vertebral compression fractures. (5) The infectious complications and probably the development of neoplasms de novo, are related to immunosuppressive therapy which impairs virtually all host defence mechanisms and alters the nature of the host's response to infective agents or other foreign antigens. (6) Because neurological symptoms and signs were usually those of behavioural changes or deterioration in intellectual performance, the neurological examination was often of little value in diagnosing the nature or even the anatomical site of the neuropathological process. (7) The possibility of an infectious origin of the neurological manifestations must be aggressively pursued even in the absence of fever and a significantly abnormal spinal fluid examination. The diagnostic error made most frequently was to ascribe neurological symptoms erroneously to metabolic disturbances or to "intensive care unit psychosis" when they were in fact due to unrecognized CNS infection. (8) maintenance of mean cardiopulmonary bypass pressures above 70 mmHg, particularly in patients with known arteriosclerosis, may reduce operative morbidity. (9) Though increased diagnostic accuracy is possible with routine use of a variety of radiological and laboratory techniques, two further requirements probably must be met before a significant reduction in the frequency of neurological complications will occur: the advent of greater immunospecificity in suppressing rejection of the grafted organ while preserving defences against infection; and a more effective armamentarium of antiviral and antifungal drugs.
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10/42. Cerebral air embolism treated by pressure and hyperbaric oxygen.

    We used pressure and hyperbaric oxygen to treat 2 patients with cerebral air embolism, occurring as the result of invasive medical procedures, and neither suffered any permanent damage detectable by clinical examination and MRI. This outcome contrasts with reports of infarct and disability among untreated victims of air embolism.
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