RESUMEN
The gold standard for quantification of pain is a person's self-report. However, we need objective parameters for pain measurement when intensive care patients, for example, are not able to report pain themselves. An increase in pain is currently thought to coincide with an increase in stress hormones. This observational study investigated whether procedure-related pain is associated with an increase of plasma cortisol, adrenaline, and noradrenaline. In 59 patients receiving intensive care after cardiac surgery, cortisol, adrenaline, and noradrenaline plasma levels were measured immediately before and immediately after patients were turned for washing, either combined with the removal of chest tubes or not. Numeric rating scale scores were obtained before, during, and after the procedure. Unacceptably severe pain (numeric rating scale ≥ 4) was reported by seven (12%), 26 (44%), and nine (15%) patients, before, during and after the procedure, respectively. There was no statistically significant association between numeric rating scale scores and change in cortisol, adrenaline, and noradrenaline plasma levels during the procedure. Despite current convictions that pain coincides with an increase in stress hormones, procedural pain was not associated with a significant increase in plasma stress hormone levels in patients who had undergone cardiac surgery. Thus, plasma levels of cortisol, adrenaline, and noradrenaline seem unsuitable for further research on the measurement of procedural pain.
Asunto(s)
Procedimientos Quirúrgicos Cardíacos , Catecolaminas/sangre , Hidrocortisona/sangre , Dolor Postoperatorio/sangre , Anciano , Cuidados Críticos , Femenino , Humanos , MasculinoRESUMEN
To reduce unintentional and avoidable adverse events in patients in hospitals in the Netherlands, a patient safety agency (VMS) programme was launched in 2008. Among the VMS topics, the programme 'optimal therapy in severe sepsis', according to the international Surviving Sepsis Campaign (SSC), aims to improve early diagnosis and treatment of sepsis to reduce sepsis mortality by 15% before the end of 2012. We analysed compliance data submitted to the international SSC database from the Netherlands and compared these data with published international SS C results. Data of 863 patients, representing 6% of the international data (n=14,209), were used for analysis. In the Netherlands, the resuscitation bundle compliance improved significantly from 7% at baseline to 27% after two years (p=0.002). Internationally, the resuscitation bundle compliance increased significantly from 11 to 31% (p.
Asunto(s)
Mortalidad Hospitalaria/tendencias , Seguridad del Paciente/normas , Sepsis/diagnóstico , Sepsis/terapia , Adulto , Diagnóstico Precoz , Adhesión a Directriz/estadística & datos numéricos , Implementación de Plan de Salud , Humanos , Países Bajos/epidemiología , Sepsis/mortalidad , Análisis de SupervivenciaRESUMEN
Intensive care units regularly have patients in whom a curative treatment plan is changed to palliative treatment. This does not only concern the medical and technical aspects, but also medical-ethical problems and questions relating to communication and organization. All these play a part in making a correct assessment. It is logical that nurses play an important part in this process as they have the most contact with the patient and his/her family. The optimalization of collaboration between doctors and nurses by means of the mutual exchange of information unique to each different discipline as well as acknowledging one another's talents and skills, forms the basis of good communication and organization concerning end-of-life decisions. It is useful to formalize this collaboration by means of multidisciplinary discussions.
Asunto(s)
Cuidados Críticos/métodos , Toma de Decisiones , Enfermeras y Enfermeros/psicología , Cuidado Terminal/métodos , Cuidado Terminal/psicología , Cuidados Críticos/psicología , Ética en Enfermería , Humanos , Unidades de Cuidados Intensivos , Cuidados Paliativos/métodos , Cuidados Paliativos/psicología , Relaciones Médico-EnfermeroRESUMEN
The purpose of the present in vivo study was to determine the role of nitric oxide (NO) in the regulation of glucose metabolism in response to endotoxin by blocking NO synthesis with N(G)-monomethyl-L-arginine (L-NMMA). In five dogs, the appearance and disappearance rates of glucose (by infusion of [6,6-(2)H(2)]glucose), plasma glucose concentration, and plasma hormone concentrations were measured on five different occasions: saline infusion, endotoxin alone (E coli, 1.0 microg/kg i.v.), and endotoxin administration plus three different doses of primed, continuous infusion of L-NMMA. Endotoxin increased rate of appearance of glucose from 13.7 +/- 1.6 to 23.6 +/- 3.3 micromol x kg(-1) x min(-1) (P < 0.05), rate of disappearance of glucose from 13.9 +/- 1.1 to 24.8 +/- 3.1 micromol x kg(-1) x min(-1) (P < 0.001), plasma lactate from 0.5 +/- 0.1 to 1.7 +/- 0.1 mmol/l (P < 0.01), and counterregulatory hormone concentrations. L-NMMA did not affect the rise in rate of appearance and disappearance of glucose, plasma lactate, or the counterregulatory hormone response to endoxin. Plasma glucose levels were not affected by endotoxin with or without L-NMMA. In conclusion, in vivo inhibition of NO synthesis by high doses of L-NMMA does not affect glucose metabolism in response to endotoxin, indicating that NO is not a major mediator of glucose metabolism during endotoxemia in dogs.
Asunto(s)
Glucemia/metabolismo , Endotoxinas/farmacología , Óxido Nítrico/fisiología , Animales , Presión Sanguínea/efectos de los fármacos , Perros , Relación Dosis-Respuesta a Droga , Inhibidores Enzimáticos/farmacología , Frecuencia Cardíaca/efectos de los fármacos , Hormonas/sangre , Cinética , Masculino , omega-N-Metilarginina/administración & dosificación , omega-N-Metilarginina/farmacologíaRESUMEN
Sufentanil is a synthetic mu-opioid receptor agonist frequently used in anesthesia and critically ill patients. To evaluate the effects of sufentanil on the inflammatory, neuroendocrine, and metabolic responses to endotoxin, we studied six dogs during saline infusion (control), during sufentanil infusion (1.5 microg . kg-1 . h-1), after endotoxin injection (1.0 microg/kg iv), and during combined endotoxin and sufentanil administration. The rate of appearance of glucose was determined by infusion of [6,6-2H2]glucose. Sufentanil depressed the endotoxin-induced increase in body temperature (36.9 +/- 0.3 vs. 40.6 +/- 0.5 degrees C, P < 0.05). Sufentanil depressed the tumor necrosis factor (TNF) response to endotoxin by approximately 60% (P < 0.01) but increased the interleukin-6 (IL-6) response by approximately 70% (P < 0.01). Sufentanil per se induced a transient neuroendocrine activation. Sufentanil also increased plasma concentrations of insulin and catecholamines after endotoxin (P < 0.05 vs. endotoxin alone) and increased plasma glucose levels by approximately 36% (from 6.1 +/- 0.1 to 8.3 +/- 0.6 mmol/l, P < 0.05 vs. endotoxin alone). Endotoxin stimulated glucose production transiently by 95% (24.2 +/- 3.2 vs. control 12.4 +/- 1.0 micromol . kg-1 . min-1, P < 0.05). Paradoxically, sufentanil inhibited this endotoxin-induced stimulation of glucose production (P < 0.05 vs. endotoxin alone). In conclusion, sufentanil modulates the response to intravenous endotoxin by dissociating the TNF and IL-6 response, increasing insulin and catecholamine levels, and depressing the increase in glucose production. Therefore, opiates alter inflammatory, endocrine, and metabolic regulation in endotoxemia.
Asunto(s)
Glucemia/metabolismo , Endotoxemia/fisiopatología , Endotoxinas/toxicidad , Hormonas/sangre , Interleucina-6/biosíntesis , Sufentanilo/farmacología , Factor de Necrosis Tumoral alfa/biosíntesis , Animales , Glucemia/efectos de los fármacos , Presión Sanguínea/efectos de los fármacos , Temperatura Corporal/efectos de los fármacos , Deuterio , Perros , Endotoxemia/inmunología , Epinefrina/sangre , Glucagón/sangre , Frecuencia Cardíaca/efectos de los fármacos , Hormonas/metabolismo , Hidrocortisona/sangre , Infusiones Intravenosas , Insulina/sangre , Interleucina-6/sangre , Masculino , Norepinefrina/sangre , Técnica de Dilución de Radioisótopos , Receptores Opioides mu/agonistas , Valores de Referencia , Sufentanilo/administración & dosificación , Factores de TiempoRESUMEN
To evaluate the effects of a standard inflammatory challenge on the dynamics of the hypothalamic-pituitary-adrenal (HPA) axis, we studied the effects of low-dose endotoxin (1.0 microgram/kg) on plasma adrenocorticotropic hormone (ACTH) and cortisol concentrations in a saline-controlled study in five awake dogs. Four hours after endotoxin or saline challenge human corticotrophin-releasing hormone (hCRH; 1.0 microgram/kg) was administered. Plasma ACTH and cortisol levels increased considerably in response to endotoxin, from 13 +/- 1 ng/l to 360 +/- 85 ng/l (p < 0.01) and from 60 +/- 20 nmol/l to 710 +/- 80 nmol/l (p < 0.01). Despite a considerable difference in ACTH and cortisol levels prior to CRH administration between both studies (p < 0.01), the absolute increase in ACTH levels induced by hCRH was not different (231 +/ 43 ng/l vs 238 +/- 45 ng/l, control vs endotoxin). Plasma cortisol levels increased significantly in the control study (from 40 +/- 10 nmol/l to 330 +/- 40 nmol/l, p < 0.01), whereas they did not change in the endotoxin study after hCRH administration (from 710 +/- 80 nmol/l to 730 +/- 70 nmol/l, ns). We conclude that the HPA-axis reacts initially to endotoxin in such a way that cortisol, but not ACTH, secretion is maximized. Therefore, a blunted cortisol response to CRH testing is part of the initial response to infection.
Asunto(s)
Hormona Liberadora de Corticotropina/farmacología , Endotoxemia/sangre , Hidrocortisona/sangre , Hormona Adrenocorticotrópica/sangre , Animales , Presión Sanguínea/efectos de los fármacos , Temperatura Corporal/efectos de los fármacos , Temperatura Corporal/fisiología , Perros , Endotoxemia/fisiopatología , Endotoxinas/toxicidad , Frecuencia Cardíaca/efectos de los fármacos , Humanos , MasculinoRESUMEN
By US standards, about half of African children are malnourished, although most appear clinically normal. It is possible that precursor supply for gluconeogenesis is limited to a greater extent in these seemingly malnourished African children than in healthy children, consequently limiting glucose production. Since in malaria peripheral glucose utilization is increased, precursor supply could play an even more critical role in maintaining glucose production in African children suffering from falciparum malaria. We studied the effect of alanine infusion (1.5 mg/kg/min) on glucose production (measured by infusion of [6,6-2H2]glucose) and plasma glucose concentration in 10 consecutive children with acute, uncomplicated falciparum malaria. By US standards, six children were below the 10th percentile of weight for height and seven were below the 10th percentile of height for age. Plasma concentrations of alanine increased during alanine infusion from 153 +/- 21 to 468 +/- 39 mumol/l, whereas plasma lactate concentrations did not change (1.4 +/- 0.2 vs. 1.3 +/- 0.2 mmol/l). Plasma glucose concentration and glucose production did not change during alanine infusion: 4.6 +/- 0.3 vs. 4.5 +/- 0.3 mmol/l and 5.8 +/- 0.4 vs. 5.7 +/- 0.3 mg/kg/min, respectively. Gluconeogenic precursor supply is sufficient for maintainance of glucose production in African children with uncomplicated malaria who are malnourished by US standards.
Asunto(s)
Alanina/farmacología , Glucemia/efectos de los fármacos , Malaria Falciparum/sangre , Trastornos Nutricionales/sangre , Enfermedad Aguda , Glucemia/biosíntesis , Glucemia/metabolismo , Niño , Preescolar , Citocinas/sangre , Femenino , Hormonas/sangre , Humanos , Malaria Falciparum/complicaciones , Masculino , Trastornos Nutricionales/complicacionesRESUMEN
The spleen is involved in endotoxin-induced interleukin-6 (IL-6) production. To quantitate the relative contribution of the spleen to endotoxin-induced IL-6 production, we studied the effect of endotoxin (1.0 microg/kg of body weight) in control dogs (n = 7) and splenectomized dogs (n = 7). Blood for analysis of tumor necrosis factor (TNF) and IL-6 was sampled from the femoral artery and the portal, hepatic, and splenic (only in controls) veins. Arterial plasma endotoxin and cortisol levels were also measured. Whole-body IL-6 production was calculated by a deconvolution technique. Splenic IL-6 production in control dogs was measured from splenic blood flow and arteriovenous concentration differences. Endotoxin levels were higher in splenectomized dogs (P < 0.05) because of a decreased distribution volume (P < 0.05) and decreased clearance of endotoxin (P < 0.05). Endotoxin-induced plasma IL-6 levels were decreased by approximately 75% in splenectomized dogs (P < 0.01), and whole-body IL-6 production rates were severalfold lower (median of 8.7 mg/4 h and range of 3.9 to 11.4 mg/4 h versus a median of 32.3 mg/4 h and a range of 22.7 to 70.2 mg/4 h) (P < 0.05). However, in control dogs splenic IL-6 production (0.6 +/- 0.2 mg/4 h) was only approximately 2% of whole-body IL-6 production. Plasma TNF levels increased in both groups (P < 0.01) but were not different between the groups. Plasma cortisol levels were slightly higher in splenectomized dogs than in control dogs (P < 0.05). In conclusion, splenectomy decreases the distribution volume and clearance rate of endotoxin. Splenectomy results in decreased endotoxin-induced IL-6 production, which is caused not by the absence of splenic IL-6 production, but by a decrease in nonsplenic IL-6 production. Therefore, the spleen is an important mediator in the complete activation of nonsplenic IL-6 production by endotoxin.
Asunto(s)
Endotoxemia/inmunología , Endotoxinas/toxicidad , Interleucina-6/biosíntesis , Animales , Perros , Retroalimentación , Hemodinámica , Hidrocortisona/sangre , Masculino , Esplenectomía , Factor de Necrosis Tumoral alfa/biosíntesisRESUMEN
Different routes of endotoxin administration have been used to mimic inflammatory and metabolic responses observed during sepsis. Because the origin of endotoxemia may affect the reactions to endotoxin, we compared the induction of tumor necrosis factor (TNF), interleukin-6 (IL-6), hormones, and glucose production after endotoxin (1.0 microg/kg Escherichia coli 0111:B4) administration into a peripheral (n = 8) versus the portal (n = 8) vein in anesthetized dogs. Prior to endotoxin, a laparotomy was performed for cannulation of hepatic vessels. To evaluate the effects of surgery and anesthesia, we also studied the effects of peripheral endotoxin administration in six awake dogs. The rate of appearance of glucose was measured by primed continuous infusion of [6,6-2H2]glucose. In anesthetized dogs, arterial concentrations of TNF and IL-6 increased after endotoxin administration (P < 0.01 vs basal; NS between groups). Net hepatic TNF production was increased after endotoxin administration (peripheral vs portal endotoxin administration: 533 +/- 177 vs 2135 +/- 1127 ng/min, both P < 0.05 vs basal; NS between groups). Net hepatic IL-6 production was stimulated only after portal endotoxin delivery (from 86 +/- 129 to 4740 +/- 1899 ng/min, P < 0.05; NS between groups). Although there were no differences in neuroendocrine activation, portal endotoxin administration resulted in decreased glucose production compared with peripheral administration (13.6 +/- 0.9 vs 16.8 +/- 1.2 micromol/kg.min, P < 0. 05). In contrast to anesthetized dogs, endotoxin increased glucose production considerably in awake dogs from 13.8 +/- 1.2 to 24.2 +/- 3.2 micromol/kg.min (P < 0.05; P < 0.05 vs anesthetized dogs). The contribution of anesthesia and surgery increased the endotoxin-induced IL-6 response by approximately 350% compared with the effect of endotoxin in awake dogs (P < 0.01). In conclusion, there are no major differences in the responses to endotoxin between peripherally treated and portally treated dogs, except for differences in glucose production. Portal delivery compared with systemic delivery of endotoxin alters hepatic metabolism through nonendocrine mechanisms, reflected in decreased glucose production. The inflammatory, endocrine, and metabolic effects of endotoxin are altered by the combination of surgery and anesthesia.