RESUMEN
BACKGROUND: Severe respiratory failure related to infection with the pandemic influenza A/H1N1 2009 virus is uncommon but possibly life-threatening. If, in spite of maximal conventional critical care, the patient's condition deteriorates, extracorporeal membrane oxygenation (ECMO) may be a life-saving procedure. METHODS: An observational study approved by the local ethics committee was carried out. Data from all patients treated with ECMO at the ECMO Center Karolinska for influenza A/H1N1 2009-related severe respiratory failure were analyzed. The main outcome measure was survival three months after discharge from our department. RESULTS: Between July 2009 and January 2010, 13 patients with H1N1 2009 respiratory failure were treated with ECMO. Twelve patients were cannulated for veno-venous ECMO at the referring hospital and transported to Stockholm. One patient was cannulated in our hospital for veno-arterial support. The median ratio of the arterial partial oxygen pressure to the fraction of inspired oxygen (P/F ratio: PaO2 /FiO2) before cannulation was 52.5 (interquartile range 38-60). Four patients were converted from veno-venous to veno-arterial ECMO because of right heart failure (three) or life-threatening cardiac arrhythmias (one). The median maximum oxygen consumption via ECMO was 251 ml/min (187-281 ml/min). Twelve patients were still alive three months after discharge; one patient died four days after discharge due to intracranial hemorrhage. CONCLUSION: Patients treated with veno-venous or veno-arterial ECMO for H1N1 2009-related respiratory failure may have a favorable outcome. Contributing factors may include the possibility of transport on ECMO, conversion from veno-venous (v-v) or veno-arterial (v-a) ECMO if necessary, high-flow ECMO to meet oxygen requirements and active surgery when needed.
Asunto(s)
Oxigenación por Membrana Extracorpórea , Subtipo H1N1 del Virus de la Influenza A , Gripe Humana/terapia , Insuficiencia Respiratoria/terapia , Adulto , Analgésicos/uso terapéutico , Estudios de Cohortes , Infección Hospitalaria/terapia , Oxigenación por Membrana Extracorpórea/efectos adversos , Oxigenación por Membrana Extracorpórea/instrumentación , Femenino , Humanos , Hipnóticos y Sedantes/uso terapéutico , Hipoxia/terapia , Gripe Humana/complicaciones , Gripe Humana/virología , Masculino , Persona de Mediana Edad , Pandemias , Embarazo , Respiración Artificial , Pruebas de Función Respiratoria , Insuficiencia Respiratoria/etiología , Insuficiencia Respiratoria/virología , Resultado del TratamientoRESUMEN
BACKGROUND: Little has been reported about intensive care of children in Sweden. The aims of this study are to (I) assess the number of admissions, types of diagnoses and length-of-stay (LOS) for all Swedish children admitted to intensive care during the years 1998-2001, and compare paediatric intensive care units (PICUs) with other intensive care units (adult ICUs) (II) assess immediate (ICU) and cumulative 5-year mortality and (III) determine the actual consumption of paediatric intensive care for the defined age group in Sweden. METHODS: Children between 6 months and 16 years of age admitted to intensive care in Sweden were included in a national multicentre, ambidirectional cohort study. In PICUs, data were also collected for infants aged 1-6 months. Survival data were retrieved from the National Files of Registration, 5 years after admission. RESULTS: Eight-thousand sixty-three admissions for a total of 6661 patients were identified, corresponding to an admission rate of 1.59/1000 children per year. Median LOS was 1 day. ICU mortality was 2.1% and cumulative 5-year mortality rate was 5.6%. Forty-four per cent of all admissions were to a PICU. CONCLUSIONS: This study has shown that Sweden has a low immediate ICU mortality, similar in adult ICU and PICU. Patients discharged alive from an ICU had a 20-fold increased mortality risk, compared with a control cohort for the 5-year period. Less than half of the paediatric patients admitted for intensive care in Sweden were cared for in a PICU. Studies are needed to evaluate whether a centralization of paediatric intensive care in Sweden would be beneficial to the paediatric population.
Asunto(s)
Cuidados Críticos/estadística & datos numéricos , Unidades de Cuidado Intensivo Pediátrico/estadística & datos numéricos , Adolescente , Distribución por Edad , Niño , Preescolar , Humanos , Lactante , Tiempo de Internación , Estaciones del Año , Tasa de Supervivencia , Suecia , Factores de Tiempo , Resultado del TratamientoRESUMEN
The objective of this study was to investigate the role of nitric oxide and oxygen in the regulation of pulmonary vascular resistance, especially by means of substitution with nitric oxide after inhibition of endogenous nitric oxide formation. In artificially ventilated open-chest rabbits pulmonary vascular resistance at normoxic ventilation (FIO2 = 21%) was 56 +/- 6 cmH2O ml-1 min-1 1000-1 (mRUL). N omega-nitro-L-arginine methyl ester (L-NAME, 30 mg kg-1), an inhibitor of NO synthase, increased pulmonary vascular resistance to 122 +/- 17 mRUL at normoxic ventilation. In response to L-NAME there was also an increase in mean arterial blood pressure. Exogenous nitric oxide (0.014-9 p.p.m. in the inhaled air) dose-dependently and reversibly counteracted the effect of L-NAME on pulmonary vascular resistance at normoxic ventilation, without affecting systemic blood pressure. In addition, the L-NAME-induced vasoconstriction was critically dependent on oxygen. Thus, during hypoxic ventilation (FIO2 = 10%) the pulmonary vascular resistance was increased approximately four-fold by the presence of L-NAME (30 mg kg-1), and increments in FIO2 (21-100%) dose-dependently and reversibly counteracted the effect of L-NAME on pulmonary vascular resistance. Taken together these findings demonstrate that inhalation of low doses of NO may act as a replacement when endogenous NO synthesis is inhibited, and that pulmonary vasoconstriction induced by NO synthesis inhibition is likely to be the result of interference with oxygen-dependent regulatory mechanisms. Endogenous NO co-operates with oxygen to evoke a vasodilator component of the pulmonary hypoxic pressor response, balancing a hitherto unknown constrictor mechanism.