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1.
J Pediatr Surg ; 57(11): 534-537, 2022 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-35181123

RESUMEN

AIM: Ultrasound-guided (USG) percutaneous insertion of Broviac lines (cuffed tunnelled silastic central venous catheters, TCVC) has increasingly been adopted throughout the UK. However, vascular access remains a challenge in small babies and in some units is still performed by open cutdown. Our vascular access team, established in 2004, consists of consultant surgeons, anaesthetists and interventional radiologists, who provide all permanent vascular access by the USG technique. We reviewed the outcome in our last 100 patients less than 5 kg. METHOD: A prospective database of TCVC insertions in patients <5 kg weight recorded age, gestation, weight, diagnosis, type of catheter and complications within 28 days of insertion. A standardised technique of USG insertion is used by all operators. RESULTS: One-hundred patients <5 kg had TCVC inserted between 1/1/2018 and 31/3/2020. Median age 46(range0-316)days, gestation 36.5(23-42)weeks, weight 3(0.66 to 5)kg. INDICATION: parenteral nutrition(75), long term antibiotics(14), cardiac medication(6), chemotherapy(3), other(2). All were tunnelled silicone lines of single 2.7fr(51) and 4.2fr(46) or double lumen 7fr(3). Uncomplicated insertion in 94/100 cases. In 6 patients difficulties were encountered with cannulating the vein. In 4 cases an experienced colleague was called and managed to cannulate the vein; in 1 case a new successful attempt was made on the opposite internal jugular vein, and in 1 the femoral vein was used. No patient required an open cutdown. There were no cases of line sepsis requiring removal but 1 replacement was required for blockage within 28days. CONCLUSION: The USG approach in infants<5 kg is safe and can be used exclusively for venous access even in the most tiny babies. It is, however, a technically challenging procedure therefore we would recommend establishing a consultant delivered vascular access team to provide this service. Open venous cutdown in a tertiary children's hospital is no longer necessary for the insertion of TCVC and should be abandoned altogether. LEVELS OF EVIDENCE: Level I Prognosis Study.


Asunto(s)
Cateterismo Venoso Central , Antibacterianos , Cateterismo Venoso Central/efectos adversos , Cateterismo Venoso Central/métodos , Catéteres de Permanencia/efectos adversos , Niño , Cisteína/análogos & derivados , Humanos , Lactante , Recién Nacido , Venas Yugulares/diagnóstico por imagen , Persona de Mediana Edad , Estudios Prospectivos , Siliconas , Ultrasonografía Intervencional/métodos
2.
Acta Neuropathol Commun ; 3: 14, 2015 Mar 24.
Artículo en Inglés | MEDLINE | ID: mdl-25853174

RESUMEN

INTRODUCTION: In early stages of Alzheimer's disease (AD), neurofibrillary tangles (NFT) are largely restricted to the entorhinal cortex and medial temporal lobe. At later stages, when clinical symptoms generally occur, NFT involve widespread limbic and association cortices. At this point in the disease, amyloid plaques are also abundantly distributed in the cortex. This observation from human neuropathological studies led us to pose two alternative hypotheses: that amyloid in the cortex is permissive for the spread of tangles from the medial temporal lobe, or that these are co-occurring but not causally related events simply reflecting progression of AD pathology. RESULTS: We now directly test the hypothesis that cortical amyloid acts as an accelerant for spreading of tangles beyond the medial temporal lobe. We crossed rTgTauEC transgenic mice that demonstrate spread of tau from entorhinal cortex to other brain structures at advanced age with APP/PS1 mice, and examined mice with either NFTs, amyloid pathology, or both. We show that concurrent amyloid deposition in the cortex 1) leads to a dramatic increase in the speed of tau propagation and an extraordinary increase in the spread of tau to distal brain regions, and 2) significantly increases tau-induced neuronal loss. CONCLUSIONS: These data strongly support the hypothesis that cortical amyloid accelerates the spread of tangles throughout the cortex and amplifies tangle-associated neural system failure in AD.


Asunto(s)
Enfermedad de Alzheimer/patología , Amiloide/metabolismo , Encéfalo/patología , Ovillos Neurofibrilares/patología , Neuronas/patología , Proteínas tau/metabolismo , Envejecimiento/metabolismo , Envejecimiento/patología , Enfermedad de Alzheimer/metabolismo , Amiloide/toxicidad , Animales , Encéfalo/metabolismo , Corteza Cerebral/patología , Modelos Animales de Enfermedad , Progresión de la Enfermedad , Hipocampo/patología , Humanos , Ratones , Ratones Transgénicos , Ovillos Neurofibrilares/metabolismo , Lóbulo Temporal/patología
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