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Cranial implant removal is recommended if implants become exposed owing to scalp necrosis after cranioplasty. However, it carries the risk of extensive bleeding, and the resultant cranial defects can cause both aesthetic and functional problems. We present a case of a scalp defect exposing a cranial prosthetic implant that was reconstructed with a local flap and salvaged using an indwelling antibiotic irrigation system. A 73-year-old man presented with scalp necrosis after undergoing cranioplasty due to intracranial hemorrhage. The cranial implant was exposed through the scalp defect. Methicillin-resistant Staphylococcus aureus was detected in the culture from the open wound. After debridement of the necrotic tissue and burring of the superficial layer of the implant, a transposition flap was used to cover the defect and an indwelling antibiotic irrigation system was installed. Continuous irrigation with vancomycin was conducted for 5 days, and intravenous vancomycin was continued for 4 weeks. The flap was in good condition at 4 months postoperatively, with no infection. The convex contour of the scalp was well maintained. The patient’s neurological status was stable. Exposed cranial implants can be salvaged with continuous antibiotic irrigation as an alternative to implant removal; thus, the risk of bleeding and possible disfigurement may be avoided.
Purpose: There have been no reports concerning the role of the aorta in explaining why blood flow is low below the diaphragm and a pressure gradient is present between central and peripheral arteries during standard cardiopul-money resuscitation (CPR). The aim of this study was to assess the morphologic changes of the descending thoracic aorta and its effect on aortic pressure during precordial chest compression in cardiac arrest victims. Methods: Twelve patients with non-traumatic cardiac arrest (8 males, mean age: 58 years) were enrolled. Transesophageal echocardiography was performed to verify the morphologic changes of the descending thoracic aorta during standard manual CPR. The pressure gradient across the maximally compressed site of the aorta was measured by pullback tracing using a pigtail catheter. Results: Focal compression and deformation of the descending thoracic aorta was uniformly observed in all patients during compression systole. The mean systolic blood pressure of the descending thoracic aorta proximal and distal to the maximally compressed site was 135±36 mmHg and 115±21 mmHg, respectively. The mean systolic pressure gradient across the maximally compressed site was 20.5±17.7 mmHg. During compression systole, the pressure gradient between the right atrium and the descending thoracic aorta proximal to the maximally compressed site during compression systole was 49±12 mmHg while pressure gradient between the right atrium and the descending thoracic aorta distal to the maximally compressed site was 29±8 mmHg. Conclusion: We found that the descending thoracic aorta was focally compressed and that a pressure gradient developed across the maximally compressed site during compression systole. This may contribute to limiting blood flow to the subdiaphragmatic region during standard manual CPR in humans.
Purpose: In the mechanism of forward blood flow during cardopulmonary resuscitation (CPR) in humans, the role of the left ventricle remains to be investigated. The aim of this study was to assess the role of the left ventricle in generating forward blood flow in humans during CPR by performing contrast echocardiography. Methods: Ten patients with non-traumatic cardiac arrest were enrolled. During CPR, a pigtail catheter was introduced to the left ventricle and a central venous catheter was introduced to the right atrium under transesophageal echocardiographic guidance. Ten (10) ml of agitated saline was injected into the left ventricle to perform contrast echocardiography during CPR. The direction of contrast flow and the presence of mitral regurgitation were assessed with a 135˚ longitudinal view. Pressures were traced in the left ventricle, the aorta, and the right atrium. Results: Forward flow toward the aorta and mitral regurgitation (MR) were visualized during compression systole on left ventricular contrast echocardiography in all patients: grade I in 1, grade 11 in 3, grade III in 4, and grade IV in 2 patients. There was no differences in the clearing times (29±24 vs 22±12 sec) or he numbers of chest compressions (53±32 vs 48±28) of the contrast from the left ventricle, the systolic left ventricular pressures (96±13 mmHg vs 126±48mmHg), the systolic aortic pressures (90±11 mmHg vs 116±58 mmHg), the diastolic aortic pressures (33±13 mmHg vs 32±9 mmHg), the coronary perfusion pressures (23±12 mmHg vs 26±8 mmHg), and the end tidal carbon dioxide tensions (13±12 mmHg vs 9±3 mmHg) between the mild MR group (MR grades I and 11) and the severe MR group (MR grades III and IV). The left ventricular ejection fraction was higher in the severe MR group than in the mild MR group. Conclusion: Mitral regurgitation on left ventricular contrast echocardiography during compression systole suggests that cardiac pumping is the dominant mechanism in generating forward blood flow during standard CPR in humans.
In general, patients with neurofibromatosis type I have a higher risk than those with other types of neurofibromatosis of developing soft-tissue sarcomas related to the nervous system. We here present a 42-year-old man with neurofibromatosis type I who developed a protruding mass over only 2 weeks. The histopathological diagnosis was epithelioid sarcoma. Epithelioid sarcomas are rare and, to the best of our knowledge, no epithelioid sarcomas have been reported in patients with neurofibromatosis type I. Radical excision of the primary lesion was performed and postoperative radiotherapy and chemotherapy administered, as is recommended for epithelioid sarcoma. Our case emphasizes that patients with neurofibromatosis type I may develop malignant tumors.