Internación prolongada en un servicio de clínica médica / Long duration of hospital stay in a clinical service

Evaluamos pacientes para identifica factores determinantes de estadía hospitalaria prolongada y complicaciones de la misma. MATERIAL Y MÉTODO: estudio retrospectivo descriptivo. Los datos se procesaron utilizando Chi' , Test de Fisher y Test T según variables. Definimos internación prolongada (IP) estadía hospitalaria igual o mayor a 10 días. RESULTADOS: se analizaron 322 pacientes. Cincuenta (15.5%) presentaron IP y 272 (84.5%) estadía < 10 días. El promedio de edad fue 63.8 para < 10 días y 66 para IP . Presentaron comorbilidades 87% en <10 días y 86% IP. Los diagnósticos de ingreso más frecuentes en < 10 días fueron patología respiratoria (25%). incluyendo neumonía (10%), infección urinaria e insuficiencia cardiaca; y en IP neumonía (20%) y patología neurológica aguda (18%) . El 46% de IP requirió cirugía vs 20.6% (p

In order to identify determining factors and complications in illness, we evaluated patients under long period hospitalization, in a Clinical Service. METHODS: retrospective and descriptive studies. Figures were evaluated by Chi-, Fisher T and Test T, thrue variables. We call long period hospitalization to a staying of 10 days or longer. RESULTS: 322 patients were evaluated. 50 (15,5%) presented (LS) and 272 < 10 days staying. Age average was 63,8 for < 10 days and 66 for (LS). Mostly of diagnosis at admission for < 10 days were respiratory dysfunction (25%) including pneumonia (10%), urinary infection and heart failure, and for LS pneumonia 20%, acute neurological disease 18 %. The 46 % of LS required surgery vs. 20,6% (p < 1,01). The LS needed parenteral nutrition 26 % vs. 12,5% (p < 0,02). The average of maximum amount of drugs/day in staying was: 5,8 for < 10 days and 8,76 for LS (p < 0,01). Hospital complications in LS were 28 % vs. 11% (p < 0,01), mainly nosocomial pneumonia (p < 0,01) and endovascular infections (p < 0,01). Staying in ICU was 54% for LS vs. 19% (p < 0,01), and average of days in intensive care unit (ICU) was 8 in LS vs. 3 (p < 0,01). There wasn't any difference in mortality. CONCLUSION: the admission's diagnosis and the ICU's staying were the main causes of LS, but not so age and co-morbilities studied. The LS patients require more complex and expensive staying. They present more hospital complications.

Enfermedad de Castleman / Castleman disease

A 66 years female, who was since last year under astenia, arthralgias, pimply lesions in spread plates and tests showing eritrosedimentation over 100 mm, anemi, leucocitosis with neutrofilia, policlonal hypergammaglobulinemia, slight proteinuria and IgE on 900. This patient was sporadically treated with corticoids. When made the medical consult had lost 34lb., was under anorexy, as well as dyspepsia. Hemoglobyn 6.9 gr/dl, leucocytes 20000/mm3, neutrofils at 90%, proteinogram the same as former, with hypoalbuminemia. She was taking prednisona, 16 mg/day. When examined showed depress of conscience, astenia, and dermic lesions already quoted. 4 cm nonpainful right axillary adenopaty adhered to deep planes. Medulogram with increased iron, hyperegenerative. Ganglionar biopsia: linfoid hyperplasic process linked to inmune response. Toracoabdominal tomography with adenomegalia in torax and retroperitoneo. Skin biopsia: neutrofilic vasculitis. The patient suspends the 16 mg of prednisona and fever as well as generalized adenopatias come up. After laying aside other ethiologies, and understanding as Castleman Multicentric disease, it is started to supply prednisona 1 mg/kg of weight with a clinical and biochemical fast and outstanding response. After 7 months it was progressively suspended the esteroids and 60 days later, the process fall back; for that, corticoids are restarted, with a good evolution. The illness of Castleman although it is not very frequent, it should be considered as differential diagnosis in those clinical cases that are accompanied with important general commitment, linphadenopaties and respons to steroid therapy.

Mujer de 66 años que un año previo a la consulta presentaba astenia, artralgias, lesiones pruriginosas y eritematosas en placa diseminadas. Eritrosedimentación mayor de 100mm, anemia, leucocitosis con neutrofilia, hipergammaglobulinemia policlonal, proteinuria leve e IgE de 900. Fue tratada esporádicamente con corticoides. Llega a la consulta con pérdida de 15kg de peso, anorexia y dispepsia. Hemoglobina 6.9gr/dl, leucocitos 20000/mm3, neutrófilos 90%, proteinograma similar al previo mas hipoalbuminemia. Recibía prednisona 16mg;día. Al examen bradipsíquica, asténica, lesiones dérmicas ya descritas, adenopatía axilar derecha de 4cm no dolorosa adherida a planos profundos. Medulograma con hierro aumentado, hiperregenerativa. Biopsia ganglionar: proceso hiperplásico linfoide relacionado a respuesta inmune. Tomografía tóracoabdominal con adenomegalias en medias tino y retroperitoneo. Biopsia de piel: vasculitis neutrofílica. Suspende el corticoide y aparece fiebre y adenopatías generalizadas. Tras descartar otras etiologías, se interpreta como Enfermedad de Castleman. Inicia prednisona a lmg/kg/ día con favorable, rápida y llamativa respuesta clínica y bioquímica. Luego de 7 meses se suspende de manera progresiva los esteroides, y a los 60 días presenta recaída por lo que se reinicia la terapéutica con una nueva favorable evolución. La enfermedad de Castleman si bien es poco frecuente, debe ser considerada como diagnóstico diferencial en aquellos cuadros clínicos que se acompañan de importante compromiso general. adenomegalias y respuesta a terapia con corticoides.