RESUMEN
Epidural or spinal anesthesia-related infections cause serious and devastating morbidity and mortality. The possible infectious complications of neuraxial anesthesia have become better understood in the past 10 years. We assessed information from published case series, studies, randomized controlled trials, and retrospective cohort studies to determine the rate of neuraxial infection and to evaluate iatrogenic causes of infection. The use of sterile gowning appears to be a factor associated with the decreased infection rates noted in some studies. A review of the literature demonstrated that personnel in interdisciplinary specialties use gowns for invasive procedures to prevent infection, and national and international multidisciplinary health care professionals appear to be increasing their use of sterile gowning to prevent infections. We undertook this literature review to explore the incidence of neuraxial infection, provide additional insight into multidisciplinary standards, and evaluate whether the use of sterile gowns while performing neuraxial anesthesia decreases infection rates.
Asunto(s)
Anestesia Epidural/efectos adversos , Anestesia Raquidea/efectos adversos , Infecciones Bacterianas/prevención & control , Complicaciones Intraoperatorias/prevención & control , Vestimenta Quirúrgica/estadística & datos numéricos , Infecciones Bacterianas/epidemiología , Humanos , Incidencia , Complicaciones Intraoperatorias/epidemiología , Estudios RetrospectivosRESUMEN
BACKGROUND: Increases in myocardial blood flow preserve myocardial oxygenation during moderate acute normovolemic hemodilution. Hypocapnic alkalosis (HA) is known to cause coronary vasoconstriction and increase hemoglobin-oxygen affinity. We evaluated whether these effects would compromise myocardial oxygenation during hemodilution. METHODS: Eighteen anesthetized dogs were studied. Myocardial blood flow (MBF) was measured with radioactive microspheres. Arterial and coronary sinus samples were analyzed for oxygen content and plasma lactate. Myocardial oxygen supply, oxygen uptake, and lactate uptake were calculated. HA (PaCO2, 23 ± 2 (SD); pHa, 7.56 ± 0.03) was induced by removal of dead space tubing at baseline (n = 8) and during hemodilution (n = 10), with hematocrit at 43 ± 4% and 19 ± 2%, respectively. RESULTS: Hemodilution during normocapnia caused decreases in arterial oxygen content (19.9 ± 2.4 to 9.3 ± 1.2 ml/100; P < 0.05) and the coronary arteriovenous 02 difference (13.0 ± 3.0 to 6.4 ± 0.9 ml/100ml; P < 0.05). MBF increased (52 ± 12 to 111 ± 36 ml/min/100g; P < 0.05) to maintain myocardial oxygen supply and oxygen uptake. Myocardial lactate uptake increased (31 ± 19 to 68 ± 35 µeq/min/100g; P < 0.05). At normal hematocrit, HA decreased MBF (57 ± 18 to 45 ± 10 ml/min/100; P < 0.05), implying vasoconstriction, accompanied by decreased myocardial oxygen supply. These myocardial effects of HA were not apparent during hemodilution. HA did not alter myocardial lactate uptake during hemodilution. CONCLUSION: When HA was induced during hemodilution, its ability to cause coronary vasoconstriction was lost, and myocardial oxygenation remained well preserved.
Asunto(s)
Alcalosis/fisiopatología , Hemodilución , Hipocapnia/fisiopatología , Miocardio/metabolismo , Oxígeno/metabolismo , Animales , Circulación Coronaria , Perros , Femenino , Masculino , VasoconstricciónRESUMEN
BACKGROUND: Hemodilution is accompanied by an increase in cerebral blood flow, but whether this is due to vasodilation in response to reduced arterial oxygen content, reduced blood viscosity, or a combination of these mechanisms is a matter of debate. We performed the current study to gain insight into this question by evaluating the effect of hemodilution on (1) vasodilator reserve and (2) the level of blood flow during hypercapnia-induced vasodilation in regions of the brain and spinal cord. METHODS: Sixteen mongrel dogs were anesthetized with halothane 0.9% (1 minimum alveolar concentration) while their lungs were mechanically ventilated. Radioactive microspheres (15 µm) were used to measure regional blood flow (RBF) in the cerebral cortex, cerebellum, pons, medulla, and spinal cord (cervical, thoracic, and lumbar segments). Arterial blood pressure was measured via an aortic catheter. Vasodilator reserve was assessed from the ratio of RBF during hypercapnia (PaCO2 approximately 65 mm Hg) to RBF before hypercapnia. PaCO2 was increased by the addition of dead-space tubing without changing the ventilator settings. The dilating effects of hypercapnia within the central nervous system (CNS) were assessed with hematocrit normal (group 1; n = 8) and after induction of isovolemic hemodilution to a hematocrit of 19 ± 4 (SD) with 5% dextran (group 2; n = 8). RESULTS: Hemodilution increased RBF (P < 0.0001) and decreased the vasodilator reserve ratio (P < 0.05) in all regions of the brain and spinal cord; the ratios during hemodilution (group 2) were only 48% to 68% of those without hemodilution (group 1). The level of RBF during hypercapnia was not significantly different in the absence and presence of hemodilution (cerebral cortex: mean, 122 mL/min/100 g vs mean, 108 mL/min/100 g; 95% confidence interval of the difference (95% CID), -53 to 26; P = 0.46; cerebellum: mean, 117 mL/min/100 g vs mean, 100 mL/min/100 g; 95% CID, -52 to 18; P = 0.32; pons: mean, 83 mL/min/100 g vs mean, 73 mL/min/100 g; 95% CID, -12 to 31; P = 0.35; medulla: mean, 96 mL/min/100 g vs mean, 82 mL/min/100 g; 95% CID, -11 to 40; P = 0.25; cervical spinal cord: mean, 61 mL/min/100 g vs mean, 52 mL/min/100 g; 95% CID, -18 to 34; P = 0.51; thoracic spinal cord: mean, 35 mL/min/100 g vs mean, 46 mL/min/100 g; 95% CID, -30 to 8; P = 0.24; lumbar spinal cord: mean, 54 mL/min/100 g vs mean, 58 mL/min/100 g; 95% CID, -25 to 15; P = 0.61). Neither hypercapnia alone nor combined with hemodilution affected mean arterial blood pressure (P = 0.78 and P = 0.81, respectively). CONCLUSIONS: Hemodilution caused recruitment of the vasodilator reserve, suggesting that vasodilation played a role in the increase in RBF throughout the CNS. Although the mean values for RBF during hypercapnia were similar with and without hemodilution, a large variation in the responses precluded a conclusive determination of whether or not reduced blood viscosity also contributed to the hemodilution-induced increases in RBF. A dependence on vasodilation would limit autoregulatory capability throughout the CNS during hemodilution, which would enhance the risk for ischemia if hypotension was superimposed.