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3.
Med. intensiva (Madr., Ed. impr.) ; 37(2): 99-109, mar. 2013. tab
Article in Spanish | IBECS | ID: ibc-113783

ABSTRACT

La Hipertensión Intraabdominal (HIA) y el Síndrome Compartimental Abdominal (SCA) son entidades frecuentes en los pacientes graves y cursan con una alta mortalidad. En esta revisión se actualizan los aspectos más debatidos sobre la HIA y el SCA: factores desencadenantes, epidemiología, pronóstico, métodos de medición de la presión intraabdominal (PIA), consecuencias fisiopatológicas y medidas terapéuticas, tanto médicas como quirúrgicas. Se plantea que, simultáneamente a los mecanismos de lesión estrictamente físicos, como la compresión directa de vasos y órganos intraabdominales, la transmisión de la PIA a otros compartimentos y el descenso del gasto cardíaco, pueden intervenir también una serie de mediadores inmunoinflamatorios generados en el propio intestino. La hipoperfusión, la isquemia mantenida y el fenómeno isquemia-reperfusión actuarían sobre la microbiota, el epitelio y sistema inmune intestinal desencadenando el Síndrome de Distrés Intestinal Agudo, una respuesta inflamatoria sistémica y una eventual disfunción multiorgánica que pueden aparecer en fases tardías del SCA (AU)


Seriously ill patients frequently present intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) as complications, and the associated mortality is very high. This review offers an update on the most controversial aspects of these entities: factors favoring their appearance, the most common causes, prognosis, and methods of measuring intra-abdominal pressure (IAP), physiopathological consequences in relation to the different organs and systems, and the currently accepted treatment measures (medical and/or surgical). Simultaneously to the strictly physical mechanisms of injury, such as direct compression of intra-abdominal organs and vessels, the transmission of IAP to other compartments, and the drop in cardiac output, a series of immune-inflammatory mediators generated in the intestine itself may also intervene. Hypoperfusion, sustained ischemia and the ischemia-reperfusion phenomenon, would act upon the microbiota, intestinal epithelium and intestinal immune system, triggering a systemic inflammatory response and multiorgan dysfunction that appears in the final stages of ACS (AU)


Subject(s)
Humans , Compartment Syndromes/complications , Intestinal Diseases/complications , Intra-Abdominal Hypertension/complications , Risk Factors , Critical Illness , Systemic Inflammatory Response Syndrome/complications
4.
Med Intensiva ; 37(2): 99-109, 2013 Mar.
Article in Spanish | MEDLINE | ID: mdl-22244213

ABSTRACT

Seriously ill patients frequently present intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) as complications, and the associated mortality is very high. This review offers an update on the most controversial aspects of these entities: factors favoring their appearance, the most common causes, prognosis, and methods of measuring intra-abdominal pressure (IAP), physiopathological consequences in relation to the different organs and systems, and the currently accepted treatment measures (medical and/or surgical). Simultaneously to the strictly physical mechanisms of injury, such as direct compression of intra-abdominal organs and vessels, the transmission of IAP to other compartments, and the drop in cardiac output, a series of immune-inflammatory mediators generated in the intestine itself may also intervene. Hypoperfusion, sustained ischemia and the ischemia-reperfusion phenomenon, would act upon the microbiota, intestinal epithelium and intestinal immune system, triggering a systemic inflammatory response and multiorgan dysfunction that appears in the final stages of ACS.


Subject(s)
Intestinal Diseases/etiology , Intra-Abdominal Hypertension/complications , Acute Disease , Humans , Intra-Abdominal Hypertension/etiology , Intra-Abdominal Hypertension/physiopathology , Intra-Abdominal Hypertension/therapy , Risk Factors , Syndrome
5.
An Pediatr (Barc) ; 63(4): 307-13, 2005 Oct.
Article in Spanish | MEDLINE | ID: mdl-16219251

ABSTRACT

OBJECTIVE: To characterize the variables that might be associated with mortality and the development of neurological deficits in children with convulsive status epilepticus. PATIENTS AND METHODS: Children older than 1 month and younger than 15 years who were admitted to the pediatric intensive care unit of a university hospital between 2001 and 2004 were reviewed. Epidemiologic and clinical factors that might be related to neurological outcome at discharge from the unit were analyzed. RESULTS: Forty-one patients (median age 24 months) were included. A total of 48.3% developed refractory convulsive status epilepticus. Six patients died (mortality 14.6%) during their intensive care unit stay and neurologic worsening was observed in 8.6% of survivors (adverse outcome in 22%). Symptomatic epilepsy was present in all patients who died and in 88.9% of those who recovered with severe neurologic sequelae. Uni- and multivariate analysis showed that adverse outcome was related to symptomatic origin and refractory convulsive status epilepticus (p < 0.05). CONCLUSIONS: Mortality and morbidity is high in childhood convulsive status epilepticus. Refractory convulsive status and symptomatic origin were markers of poor outcome. Children who did not have symptomatic epilepsy had a favorable outcome.


Subject(s)
Status Epilepticus/complications , Status Epilepticus/mortality , Child , Child, Preschool , Cohort Studies , Female , Humans , Infant , Male , Prognosis , Retrospective Studies
6.
An. pediatr. (2003, Ed. impr.) ; 63(4): 307-313, oct. 2005. tab
Article in Es | IBECS | ID: ibc-044170

ABSTRACT

Objetivo: Investigar las variables que se asocian a la mortalidad y al desarrollo de secuelas neurológicas en los niños con estado epiléptico convulsivo. Pacientes y métodos: Revisión de los casos con estado epiléptico convulsivo, en niños mayores de un mes y menores de 15 años, tratados en la unidad de cuidados intensivos pediátricos de un hospital universitario entre los años 2001 y 2004. Se analizaron factores epidemiológicos y clínicos en relación con el estado neurológico al alta de la unidad. Resultados: Se incluyeron 41 pacientes con una edad mediana de 24 meses. El 43,9 % desarrolló estado epiléptico convulsivo refractario. Fallecieron 6 pacientes (mortalidad: 14,6 %) y en el 8,6 % de los supervivientes se observó un deterioro neurológico con respecto a su situación previa (mala evolución en el 22 %). Todos los pacientes que fallecieron y el 88,9 % de los que presentaron secuelas graves eran portadores de formas sintomáticas. El análisis univariante y multivariante reflejaron que la etiología sintomática y el estado epiléptico refractario se asociaron con un mal pronóstico (p < 0,05). Conclusiones: La morbimortalidad del estado epiléptico convulsivo es elevada y se relaciona con la etiología sintomática y con el desarrollo de resistencia al tratamiento. Los niños que no presentan un estado epiléptico convulsivo de tipo sintomático presentan un pronóstico favorable


Objective: To characterize the variables that might be associated with mortality and the development of neurological deficits in children with convulsive status epilepticus. Patients and methods: Children older than 1 month and younger than 15 years who were admitted to the pediatric intensive care unit of a university hospital between 2001 and 2004 were reviewed. Epidemiologic and clinical factors that might be related to neurological outcome at discharge from the unit were analyzed. Results: Forty-one patients (median age 24 months) were included. A total of 48.3 % developed refractory convulsive status epilepticus. Six patients died (mortality 14.6 %) during their intensive care unit stay and neurologic worsening was observed in 8.6 % of survivors (adverse outcome in 22 %). Symptomatic epilepsy was present in all patients who died and in 88.9 % of those who recovered with severe neurologic sequelae. Uni- and multivariate analysis showed that adverse outcome was related to symptomatic origin and refractory convulsive status epilepticus (p < 0.05). Conclusions: Mortality and morbidity is high in childhood convulsive status epilepticus. Refractory convulsive status and symptomatic origin were markers of poor outcome. Children who did not have symptomatic epilepsy had a favorable outcome


Subject(s)
Infant , Child , Child, Preschool , Humans , Status Epilepticus/complications , Status Epilepticus/mortality , Cohort Studies , Prognosis , Retrospective Studies
7.
An Esp Pediatr ; 56(2): 99-103, 2002 Feb.
Article in Spanish | MEDLINE | ID: mdl-11827669

ABSTRACT

OBJECTIVE: To describe abnormalities in coagulation and fibrinolysis in septic shock with purpura and to assess the relationship between plasma plasminogen activator inhibitor-1 (PAI-1) concentrations and multiple organ system failure (MOSF). METHODS: Observational study in the pediatric intensive care unit of a tertiary care hospital. The presence of early MOSF was assessed at admission in 15 children with septic shock and purpura consecutively admitted to the pediatric intensive care unit. Blood samples were taken to determine coagulation and fibrinolysis parameters. RESULTS: At admission, MOSF was diagnosed in 7 patients (46.7 %), acute respiratory distress syndrome (ARDS) in 6 (40 %), consumption coagulopathy in 7 (46.7 %) and acute renal failure in 1 (6.7 %). The overall mortality rate was 40 %. Coagulation parameters were generally affected but statistically significant differences were found only in concentrations of fibrinogen and antithrombin III, which were lower in patients with MOSF than in those without organ dysfunction. Fibrinolysis parameters were increased in all patients but plasma PAI-1 concentrations were significantly elevated only in patients with MOSF and in those with ARDS. CONCLUSION: These data indicate that impaired fibrinolysis could play a major role in the development of MOSF in children with septic shock and purpura.


Subject(s)
Blood Coagulation , Multiple Organ Failure/etiology , Purpura/etiology , Shock, Septic/complications , Child , Child, Preschool , Female , Fibrinolysis , Humans , Infant , Male , Multiple Organ Failure/blood , Plasminogen Activator Inhibitor 1/blood , Purpura/blood , Shock, Septic/blood
8.
An. esp. pediatr. (Ed. impr) ; 56(2): 99-103, feb. 2002.
Article in Es | IBECS | ID: ibc-5117

ABSTRACT

Objetivos: Describir las alteraciones en el sistema de la coagulación y la fibrinólisis en el shock séptico asociado a púrpura y analizar la relación entre concentración plasmática de inhibidor del activador del plasminógeno tipo 1 (PAI-1) y la presencia de fracaso multiorgánico (FMO). Métodos: Estudio observacional en la Unidad de Cuidados Intensivos Pediátricos (UCIP) de un hospital universitario de tercer nivel. Se analizó en 15 niños ingresados de forma consecutiva con shock séptico y púrpura la presencia de FMO en el momento del ingreso. Se obtuvieron muestras sanguíneas para estudiar los parámetros del sistema de coagulación y la fibrinólisis. Resultados: En el momento del ingreso 7 pacientes (46,7%) presentaban FMO; 6 pacientes (40%), síndrome de distrés respiratorio agudo (SDRA); 7 pacientes (46,7%), coagulopatía de consumo, y 1 paciente (6,7%), fracaso renal agudo. La mortalidad observada fue de 40%. Los parámetros del sistema de la coagulación analizados estaban en general alterados, aunque sólo se observaron diferencias estadísticamente significativas en las concentraciones plasmáticas de fibrinógeno y antitrombina III que fueron menores en el grupo con FMO que en los pacientes sin disfunción de órganos. Los parámetros de la fibrinólisis estaban aumentados en todos los pacientes pero sólo se observaron concentraciones plasmáticas de PAI-1 significativamente elevadas en el grupo con FMO y en aquellos con SDRA. Conclusiones: Los resultados sugieren que las alteraciones del sistema fibrinolítico pueden tener un papel importante en el desarrollo de FMO en niños con shock séptico y púrpura (AU)


Subject(s)
Child , Child, Preschool , Male , Infant , Female , Humans , Blood Coagulation , Shock, Septic , Plasminogen Activator Inhibitor 1 , Multiple Organ Failure , Purpura , Fibrinolysis
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