Recomendaciones prácticas para el manejo perioperatorio del paciente con sospecha o infección grave por coronavirus SARS-CoV-2 / Practical recommendations for the perioperative management of the patient with suspection or serious infection by coronavirus SARS-CoV

En diciembre del 2019, la Comisión Municipal de Salud y Sanidad de Wuhan (provincia de Hubei, China) informó de una serie de casos de neumonía de etiología desconocida. El 7 de enero del 2020, las autoridades chinas identificaron como agente causante del brote un nuevo tipo de virus de la familia Coronaviridae, denominado SARS-CoV-2. Desde entonces, se han notificado miles de casos con una diseminación global. Las infecciones en humanos provocan un amplio espectro clínico que va desde infección leve del tracto respiratorio superior, hasta síndrome de distrés respiratorio agudo grave y sepsis. No existe un tratamiento específico para SARS-CoV-2, motivo por lo que los aspectos fundamentales son establecer medidas adecuadas de prevención y el tratamiento de soporte y manejo de las complicaciones

In December 2019, the Wuhan Municipal Health and health Commission (Hubei Province, China) reported a series of cases of pneumonia of unknown etiology. On January 7, 2020, the Chinese authorities identified as a causative agent of the outbreak a new type of virus of the Coronaviridiae family, called SARS-CoV-2. Since then, thounsands of cases have been reported with global dissemination. Infections in humans cause a broad clinical spectrum ranging from mild upper respiratory tract infection, to severe acute respiratory distress syndrome and sepsis. There is not specific treatment for SARS-CoV-2, which is why the fundamental aspects are to establish adequate prevention measures and support treatment and management of complications

Practical recommendations for the perioperative management of the patient with suspection or serious infection by coronavirus SARS-CoV. / Recomendaciones prácticas para el manejo perioperatorio del paciente con sospecha o infección grave por coronavirus SARS-CoV-2.

In December 2019, the Wuhan Municipal Health and health Commission (Hubei Province, China) reported a series of cases of pneumonia of unknown etiology. On January 7, 2020, the Chinese authorities identified as a causative agent of the outbreak a new type of virus of the Coronaviridiae family, called SARS-CoV-2. Since then, thounsands of cases have been reported with global dissemination. Infections in humans cause a broad clinical spectrum ranging from mild upper respiratory tract infection, to severe acute respiratory distress syndrome and sepsis. There is not specific treatment for SARS-CoV-2, which is why the fundamental aspects are to establish adequate prevention measures and support treatment and management of complications.

Plasma and peritoneal fluid population pharmacokinetics of micafungin in post-surgical patients with severe peritonitis.

OBJECTIVES: Limited information about the pharmacokinetics of micafungin in the peritoneal cavity is available. The aim of this study was to explore the pharmacokinetics/pharmacodynamics of micafungin in plasma and peritoneal fluid in post-surgical critically ill patients with proven or suspected intra-abdominal fungal infection. METHODS: Patients were administered 100 mg/day micafungin. Serial blood and peritoneal fluid samples were collected on day 1 and day 3 (steady-state) of treatment. Concentrations were determined by validated chromatography and were subject to a population pharmacokinetic analysis with Pmetrics(®). Monte Carlo simulations were performed for AUC0-24/MIC ratios in plasma. The PTA was calculated using AUC0-24/MIC cut-offs: 285 for Candida parapsilosis and 3000 for non-parapsilosis Candida spp. RESULTS: Ten patients were included; six were male. The median (range) age, APACHE II score and Mannheim peritonitis index were 72 (43-85) years, 15 (11-36) and 26 (8-37), respectively. On day 1, median (SD) penetration of micafungin into the peritoneal cavity was 30% (30%-40%). A three-compartment model adequately described the data. The mean (SD) estimates for clearance and volume of distribution of the central compartment were 1.27 (0.75) L/h and 9.26 (1.11) L, respectively. In most patients, the PTA in plasma was ≥ 90% for MICs of 0.008-0.016 mg/L for Candida spp. and 0.125-0.25 mg/L for C. parapsilosis. CONCLUSIONS: After the first dose, micafungin at 100 mg/day achieves pharmacokinetic/pharmacodynamic targets in plasma for Candida spp. and C. parapsilosis MICs of 0.008-0.016 and 0.125-0.25 mg/L, respectively.

Estudio comparativo de dosis bajas de bupivacaína hiperbárica versus convencionales para cesárea programada: reflexiones / On the randomized trial comparing low dose and conventional hyperbaric bupivacaine for cesarean section

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INTRODUCTION:Spinal anesthesia is the technique most often applied in cases of scheduled cesarean section.Many authors have tried decreasing the local anesthetic dose by adding opioids to achieve adequate analgesia with greater hemodynamic stability,although the ideal dose remains to be established.Our aim was to analyze hemodynamic stability and quality of analgesia with 2 different regimens for administering spinal hyperbaric bupivacaine. METHODS:We designed a controlled,double-blind trial comparing 2 doses of spinal hyperbaric bupivacaine with fentanyl in 42 patients undergoing elective cesarean sec- tion randomized to 2 groups to receive either the low dose or the conventional one.One group received an 11 mg dose of bupivacaine and the other group received a 6.5 mg dose,combined with 20 g of fentanyl in both cases. RESULTS:The hemodynamic profile and the level of maximum sensory block obtained were similar in the two groups.The motor block was less intense in patients receiving the lower dose and it was necessary to convert 2 patients (10%)to general anesthesia in that group. CONCLUSIONS:Spinal anesthesia with low doses of bupivacaine and fentanyl provides acceptable intraopera- tive conditions for a high percentage of patients under- going cesarean section,with a similar incidence of hypo- tension.The low dose generates a less intense intraoperative motor blockade with similar spread of the sensory block.The low dose was not efficacious for 10% of the patients who received it

Dexmedetomidine modulates cardiovascular responses to stimulation of central nervous system pressor sites.

UNLABELLED: Halothane attenuates the alterations in arterial pressure (BP) and heart rate (HR) produced by central nervous svstem (CNS) stimulation. We examined the effects of the alpha2-adrenergic agonist dexmedetomidine, with and without halothane, on cardiovascular regulation during CNS pressor site stimulation in chronically instrumented cats. Stimuli trains via bipolar stimulating electrodes in the hypothalamus and reticular formation elicited pressor responses. Dexmedetomidine-induced (15 microg/kg PO) bradycardia was greater in the presence of halothane. CNS stimulation increased BP and HR, which were dose-dependently attenuated by halothane (hypothalamic stimulation 71 +/- 9 mm Hg at control, 25 +/- 5 and 15 +/- 3 mm Hg at 1.0% and 1.5% halothane, respectively). Although dexmedetomidine alone did not alter pressor responses, halothane plus dexmedetomidine attenuated pressor responses in a potentially synergistic fashion (hypothalamic stimulation 67 +/- 8 mm Hg at control, 2 +/- 1 and 1 +/- 0.4 mm Hg at 1.0% and 1.5% halothane, respectively). These results suggest differences in the disruptive effects of CNS-mediated cardiovascular responses by halothane and dexmedetomidine, and that dexmedetomidine has an anesthetic-sparing effect on these CNS-mediated cardiovascular control mechanisms, potentiating the depressant effect of halothane. IMPLICATIONS: A new potential anesthetic adjunct, dexmedetomidine, does not attenuate brain-mediated increases in blood pressure, but the combination of dexmedetomidine and the anesthetic halothane acts to modulate central cardiovascular responses.

Pharmacy savings generated by preoperative administration of clonidine.

STUDY OBJECTIVE: To evaluate the effects of the preoperative administration of clonidine by the oral, intramuscular (i.m.), or epidural routes, on isoflurane expense during total abdominal hysterectomy. DESIGN: Randomized, double-blind, placebo-controlled study. SETTING: University hospital. PATIENTS: 80 ASA physical status I and II patients scheduled for total abdominal hysterectomy. INTERVENTIONS: Patients were distributed into four groups of treatment: oral, i.m., epidural, and control. Each group received 300 microg clonidine according to the treatment group, plus placebo by the other routes. The control group received placebo by all three routes. Depth of anesthesia was evaluated by changes in blood pressure and heart rate over baseline values. Cost evaluation was based on three components: expense of isoflurane, cost of 300 microg of clonidine (tablets or ampoules), and the disposable material required to dispense clonidine to each group. MEASUREMENTS AND MAIN RESULTS: Groups were comparable regarding demographic data, duration of surgery, and time to discharge from recovery room. Postoperatively, none of the patients had recall of intraoperative events. Clonidine reduced isoflurane pharmacy cost by approximately 45%, regardless of the route of administration. However, when cost of clonidine and the disposable equipment used for its administration were taken into account, the cost of the epidural kit surmounted the savings in isoflurane expense. CONCLUSION: In the patient population studied, premedication with 300 microg oral, i.m., or epidural clonidine, similarly and significantly reduced the expense of isoflurane during general anesthesia of an approximate duration of two hours. However, the cost of the epidural kit offsets the savings in isoflurane.

In vivo effects of dexmedetomidine on laser-Doppler flow and pial arteriolar diameter.

BACKGROUND: The alpha2-adrenergic agonist dexmedetomidine alters global cerebral blood flow (CBF). However, few studies have investigated the action of dexmedetomidine on the cerebral microcirculation. This investigation examined the effects of dexmedetomidine on (1) regional CBF in the rat cerebral cortex using laser-Doppler flowmetry and (2) on pial arteriolar diameter. METHODS: Halothane-anesthetized rats were fitted with instruments to measure CBF as determined by laser-Doppler flow (CBFldf) or to measure pial arteriolar diameter by preparing a cranial hollow deepened until a translucent plate of skull remained, thereby maintaining the integrity of the cranial vault. In both groups, 20 microg/kg dexmedetomidine was infused intravenously. Thirty minutes later, the mean arterial pressure was restored to control values with an infusion of phenylephrine (0.5 to 5 microg/kg/min). RESULTS: Administration of dexmedetomidine was associated with decreases in end-tidal and arterial carbon dioxide. The CBFldf and pial arteriolar diameter were measured during normocapnia (controlled carbon dioxide) and during dexmedetomidine-induced hypocapnia. Intravenous administration of dexmedetomidine significantly decreased systemic arterial pressure concurrent with a decrease in CBFldf (22% in normocapnic animals, 36% in hypocapnic animals). Restoration of mean arterial pressure increased CBFldf in normocapnic but not in hypocapnic animals. Similarly, dexmedetomidine significantly reduced pial vessel diameter in both normocapnic (9%) and hypocapnic animals (17%). However, vessel diameters remained decreased in the normocapnic and hypocapnic animals after the mean arterial pressure was restored. CONCLUSIONS: These results suggest a modulation of cerebral vascular autoregulation by dexmedetomidine which may be mediated, in part, by alterations in carbon dioxide. Dexmedetomidine may have a direct action on the cerebral vessels to reduce the CBF during normo- or hypocapnia. The differences between CBFldf and pial arteriole responses to restoration of mean arterial pressure may reflect the difference in measurement techniques because laser-Doppler measurements reflect the net effect of several arterial segments on microvascular perfusion, whereas diameter measurements specifically examined individual pial arterioles, suggesting that dexmedetomidine vasoconstriction in the cerebral vasculature may be differentially and regionally mediated.

Comparative assessment of the anaesthetic and analgesic effects of intramuscular and epidural clonidine in humans.

PURPOSE: The aim of the study was to assess and compare in analogous controlled experimental conditions, the anaesthetic sparing and analgesic effects of the same dose of clonidine administered by the intramuscular (im) and epidural (ep) routes. METHODS: We used a randomized, double blind and placebo controlled protocol. Sixty patients undergoing abdominal hysterectomy were distributed into three groups who, 30 min before surgical incision, received: 300 micrograms ep clonidine plus im saline; ep saline plus 300 micrograms im clonidine; or ep and im saline (ss). General anaesthesia was maintained with 60% N2O in O2, and isoflurane administered at concentrations to maintain mean arterial pressure (MAP) and heart rate (HR) within 20% of basal values. Isoflurane requirements (mass spectrometry), cardiovascular variables (MAP, HR), and plasma concentrations of glucose, cortisol and prolactin were evaluated at critical time points. In the recovery room (RR), sedation (Ramsay) and pain intensity (VAS) were estimated at the time of analgesia request (TAR). RESULTS: Intramuscular and ep clonidine decreased isoflurane requirements similarly by about 85% (P < 0.001). Patients in the ep group had lower MAP (P < 0.03) and HR (P < 0.001) than in the im group, but im and ep clonidine similarly blunted the plasma prolactin increase induced by intubation. In RR, ep but not im clonidine (P < 0.01) induced postoperative analgesia demonstrated by a prolonged TAR 80.8 +/- 7.3 (ep) 35.9 +/- 3.2 (im) and 44.5 +/- 5.1 (ss) min and a lower VAS (P < 0.05). CONCLUSIONS: Epidural and intramuscular clonidine decreased isoflurane requirements similarly, but only the epidural route provided postoperative analgesia, suggesting a spinal site for the analgesic action.

The effects of halothane on cardiovascular responses in the neuraxis of cats. Influence of background anesthetic state.

BACKGROUND: This study examined the effects of halothane on arterial pressure after central nervous system (CNS) pressor site stimulation in anesthetized cats, cats rendered unconscious by midcollicular transection, and conscious cats. METHODS: Two anesthetized groups and two nonanesthetized groups were used. Cats were anesthetized with either alpha-chloralose and urethane or pentobarbital. Nonanesthetized groups were cats with midcollicular transections or conscious cats with chronically implanted electrodes. Stimulating electrodes were placed into vasomotor areas of the hypothalamus (HYP), reticular formation (RF), and medulla, and arterial pressure responses to increasing stimulus currents were examined during different halothane concentrations. Two groups of cats were also anesthetized with either pentobarbital or urethane and underwent bilateral carotid artery occlusion. RESULTS: Stimulation at each CNS site produced increases in arterial pressure and heart rate. Halothane attenuated pressor responses evoked by stimulation of all loci in all groups of cats. The inhibition by halothane on these cardiovascular responses was greatest at HYP and RF sites, while the medulla was more resistant to the effects of halothane in the anesthetized animals. Midcollicular transection decreased this medullary resistance. The inhibition of pressor responses by halothane was also greater in pentobarbital-than chloralose urethane-anesthetized animals. In contrast, pressor responses elicited by bilateral carotid occlusion were attenuated by halothane similarly in both anesthetic groups. Reticular formation stimulation in conscious animals resulted in "altering responses" in addition to pressor effects, both of which were attenuated by halothane. CONCLUSIONS: Modulation of CNS cardiovascular control centers contribute to halothane-induced hemodynamic alterations. Baseline anesthesia, CNS stimulation site, and the suprabulbar system influence the effects of halothane.

The effect of clonidine on intra-operative requirements of fentanyl during combined epidural/general anaesthesia.

The study evaluates the analgesic effects of epidural clonidine in patients undergoing abdominal hysterectomy under combined epidural/general anaesthesia. Forty ASA 1-2 patients were divided into two groups who received epidurally either clonidine 300 micrograms (group 1) or placebo (group 2). Anaesthesia was maintained with oxygen/nitrous oxide, a midazolam infusion, vecuronium, and boluses of fentanyl 100 micrograms administered as needed to maintain cardiovascular stability. The mean (SD) intraoperative fentanyl requirements were 2.05 (0.18) and 3.66 (0.3) micrograms.kg-1.h-1 for groups 1 and 2 respectively (p < 0.001). Patients in Group 1 had a lower heart rate after tracheal intubation and surgical incision (p < 0.02). In the recovery room, pain intensity was lower in group 1 (p < 0.003) and the mean (SD) time until analgesia request was increased from 48.5 (8.4) min in group 2 to 235.7 (33.2) min in group 1 (p < 0.001). Our results demonstrate that epidural clonidine produces decreased fentanyl requirements, improved cardiovascular stability, reduced pain intensity and effective postoperative analgesia in the recovery room.

The effects of halothane on pressor and depressor responses elicited via the somatosympathetic reflex: a potential antinociceptive action.

The specific stimulation of various somatic sensory afferent nerves results in significant changes in autonomic responses, including systemic arterial pressure (AP) and heart rate (HR). These reflexively mediated responses have been termed the "somatosympathetic reflex" (SSR). The SSR is mediated at spinal and supraspinal sites within the central nervous system (CNS), and may, in part, represent a nociceptive response. The present investigation examined the actions of the volatile anesthetic, halothane, on the SSR evoked by electrical stimulation of peripheral nerves resulting in pressor or depressor alterations in AP and associated changes in HR. Experiments were completed in rats anesthetized with alpha-chloralose (50 mg/kg) and urethane (500 mg/kg) and mechanically ventilated. After nerve isolation, either the tibial nerve or the sciatic nerve was stimulated 1, 2, and 4 times the voltage threshold required to elicit a change in hemodynamics. Cardiovascular responses to nerve stimulation were recorded prior to, during, and after increasing concentrations of halothane (0.25%, 0.5%, and 1.0%). Halothane, as expected, produced dose-dependent decreases in AP and HR as compared to baseline controls. Electrical stimulation of the tibial nerve during control resulted in graded decreases in mean arterial pressure (MAP) with increasing current densities. Halothane significantly attenuated the depressor response to tibial nerve stimulation (decrease in MAP at maximal stimulation: 3 +/- 2 mm Hg with 1.0% halothane vs 21 +/- 2 mm Hg during control). Stimulation of the sciatic nerve resulted in current-dependent increases in AP which were significantly inhibited in the presence of halothane (increase in MAP at maximal stimulation: 7 +/- 3 mm Hg with 1.0% halothane vs 34 +/- 5 mm Hg during control).(ABSTRACT TRUNCATED AT 250 WORDS)