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Biomedical subjects

R Chioléro

Publications and source records attributed to R Chioléro.

At least 37 records · Page 2Linked to original sources
PubMed2000

Pain location, distribution, and intensity after cardiac surgery.

STUDY OBJECTIVES: To study the location, distribution, and intensity of pain in a sample of adult cardiac surgery patients during their postoperative hospital stay. DESIGN: In a prospective study, pain location, distribution (number of pain areas per patient), and intensity (0 to 10 numerical rating scale) were documented on the first, second, third, and seventh postoperative day (POD). Patient characteristics (age, sex, size, and body mass index) were analyzed for their impact on pain intensity. SETTING: A university hospital. PATIENTS: Two hundred consecutive adult patients who underwent median sternotomy for open heart surgery. There were 121 male and 79 female patients, with a mean (+/- SD) age of 60.9 +/- 19.2 years. MEASUREMENT AND RESULTS: The maximal pain intensity was significantly higher on POD 1 and 2 (3.7 +/- 2 and 3.9 +/- 1.9, respectively) and lower on POD 3 and 7 (3.2 +/- 1.5 and 2.6 +/- 1.8, respectively). The pain distribution did not vary significantly throughout the hospital stay, but the location did, with more shoulder pain on POD 7. Only age was found to have an impact on pain intensity, with patients < 60 years having a higher pain intensity than older patients on POD 2 (4.3 +/- 2.2 vs 3.6 +/- 2.4; p = 0.02). CONCLUSIONS: In this patient population, the pain intensity diminished from POD 3 onward, although its distribution did not vary significantly during the first postoperative week. Moreover, pain location changed with time, with more osteoarticular type pain at the end of the first postoperative week. Among the patients' characteristics, only younger age had an impact on pain intensity, with a higher value on POD 2.

Adolescent↗
PubMed2000

Mechanisms of postprandial hyperglycemia in liver transplant recipients: comparison of liver transplant patients with kidney transplant patients and healthy controls.

Impaired glucose tolerance or diabetes mellitus are frequent complications after organ transplantation, and are usually attributed to glucocorticoid and immunosuppressive treatments. Liver transplantation results in total hepatic denervation which may also affect glucoregulation. We therefore evaluated postprandial glucose metabolism in a group of patients with liver cirrhosis before and after orthotopic liver transplantation. Seven patients with liver cirrhosis of various etiologies, 6 patients having received a kidney transplant, and 6 healthy subjects were studied. Their glucose metabolism was evaluated in the basal state and over 4 hours after ingestion of a glucose load with 6.6 (2) H glucose dilution analysis. The patients with liver cirrhosis were studied before, and again 4 weeks (range 2-6) and 38 weeks (range 20-76, n=6) after orthotopic liver transplantation. Basal glucose metabolism was similar in liver and kidney transplant recipients. Impaired glucose tolerance was present in both groups, but postprandial hyperglycemia was exaggerated and lasted longer in liver transplant patients. Postprandial insulinemia was lower in liver transplant recipients, while C-peptide concentrations were comparable to those of kidney transplant recipients, indicating increased insulin clearance. Glucose turnover was not altered in both groups of patients during the initial 3 hours after glucose ingestion, but was higher in liver transplant early after transplantation during the fourth hour. Postprandial hyperglycemia remained unchanged in liver transplant recipients 38 weeks after liver transplantation, despite substantial reduction of immunosuppressive and glucocorticoid doses. We conclude that liver transplant recipients have severe postprandial hyperglycemia which can be attributed to insulinopenia (secondary, at least in part, to increased insulin clearance) and a late increased glucose turnover. These changes may be secondary to hepatic denervation.

Adult↗
PubMed2000

[Vasospasm treatment in intensive care].

Vasopasm is a dreadful complication of SAH associated with an important mortality and morbidity. Therapy begins with adequate monitoring and lines, and prevention of secondary brain injuries. 3-H therapy (hypervolemia--hypertension--hemodilution--hyperdynamism) aims to increase perfusion in ischemia areas. 3-H therapy is associated with systemic complication precluding it's prophylactic use. Calcium antagonists, in particular nimodipine, improve outcome and parenteral route is better than oral administration. Tirilazad seems to improve outcome of severe grades. Numerous experiments are performed with drugs interfering with the biochemical cascade leading to vasospasm, but up to today no drug is used in current clinical practice. Intraaortic balloon is still considered as experimental and may have a role in patients presenting with concomitant cardiac failure. Invasive radiology must be considered in vasospasm not improving with standard therapies. Vasopasm is a dire complication after SAH. Support and specific therapies allow a 3-fold reduction in morbidity associated with vasospasm. Vasospasm is a vital emergency, and intervention has to be quick and aggressive.

Calcium Channel Blockers↗
PubMed1999

Hepatic nonoxidative disposal of an oral glucose meal in patients with liver cirrhosis.

Seven patients with liver cirrhosis and five healthy subjects were studied over 4 hours after ingestion of a glucose meal to determine whether alterations of hepatic nonoxidative glucose disposal participate in the pathogenesis of impaired glucose tolerance. Hepatic uridyl-diphosphoglucose (UDPG) turnover was calculated from the isotopic enrichment of urinary acetaminophen glucuronide during continuous infusion of 13C-galactose and used as an index of hepatic glycogen synthesis. Patients with cirrhosis had postprandial hyperglycemia and decreased glucose clearance, but hepatic UDPG turnover was not altered (1.84 +/- 0.29 mg/kg fat-free mass min v 1.76 +/- 0.15 in controls, nonsignificant). It is concluded that hepatic postprandial glycogen synthesis is unaltered in patients with advanced cirrhosis, demonstrating important hepatic functional reserve.

Adult↗
PubMed1999

Enteral nutrition in intensive care patients: a practical approach.

Severe protein-calorie malnutrition is a major problem in many intensive care (ICU) patients, due to the increased catabolic state often associated with acute severe illness and the frequent presence of prior chronic wasting conditions. Nutritional support is thus an important part of these patient's management. Over the years, enteral nutrition (EN) has gained considerable popularity, due to its favorable effects on the digestive tract and its lower cost and rate of complications compared to parenteral nutrition. However, clinicians caring for ICU patients are often faced with contradictory data and difficult decision-making when having to determine the optimal timing and modalities of EN administration, estimation of patient requirements and choice of formulas. The purpose of this paper is to provide practical guidelines on these various aspects of enteral nutritional support, based on presently available evidence.

Contraindications↗
PubMed1999

Effect of major hepatectomy on glucose and lactate metabolism.

BACKGROUND: The liver plays an important role in glucose and lactate metabolism. Major hepatectomy may therefore be suspected to cause alterations of glucose and lactate homeostasis. METHODS: Thirteen subjects were studied: six patients after major hepatectomy and seven healthy subjects who had fasted overnight. Glucose turnover was measured with 6,6(2)H glucose. Lactate metabolism was assessed using two complementary approaches: 13C-glucose synthesis and 13CO2 production from an exogenous 13C-labeled lactate load infused over 15 minutes were measured, then the plasma lactate concentrations observed over 185 minutes after lactate load were fitted using a biexponential model to calculate lactate clearance, endogenous production, and half-lives. RESULTS: Three to five liver segments were excised. Compared to healthy controls, the following results were observed in the patients: 1) normal endogenous glucose production; 2) unchanged 13C-lactate oxidation and transformation into glucose; 3) similar basal plasma lactate concentration, lactate clearance, and lactate endogenous production; 4) decreased plasma lactate half-life 1 and increased half-life 2. CONCLUSIONS: Glucose and lactate metabolism are well maintained in patients after major hepatectomy, demonstrating a large liver functional reserve. Reduction in the size of normal liver parenchyma does not lead to hyperlactatemia. The use of a pharmacokinetic model, however, allows the detection of subtle alterations of lactate metabolism.

Adult↗
PubMed1999

Autoregulation of glucose production in health and disease.

Plasma glucose concentration is a major regulator of glucose production in experimental animals and in humans. Hyperglycemia inhibits and hypoglycemia stimulates glucose production through mechanisms which are, in part, independent of changes in glucoregulatory hormones. Glucose production does not change when gluconeogenesis is acutely inhibited or stimulated. These observations indicate an autoregulatory process by which hepatic glucose production is altered as a direct consequence of changes in glycemia. Data obtained in patients with glucokinase gene mutations indicate that glucokinase may play a role in this regulatory process. Hyperglycemia in type 2 diabetic patients and in critically ill patients may result from a blunted effect of hyperglycemia on glucose production.

Animals↗
PubMed1998

Enteral nutrition in intensive care patients: a practical approach. Working Group on Nutrition and Metabolism, ESICM. European Society of Intensive Care Medicine.

Severe protein-calorie malnutrition is a major problem in many intensive care (ICU) patients, due to the increased catabolic state often associated with acute severe illness and the frequent presence of prior chronic wasting conditions. Nutritional support is thus an important part of the management of these patients. Over the years, enteral nutrition (EN) has gained considerable popularity, due to its favorable effects on the digestive tract and its lower cost and rate of complications compared to parenteral nutrition. However, clinicians caring for ICU patients are often faced with contradictory data and difficult decisions when having to determine the optimal timing and modalities of EN administration, estimation of patient requirements, and choice of formulas. The purpose of this paper is to provide practical guidelines on these various aspects of enteral nutritional support, based on presently available evidence.

Cost-Benefit Analysis↗
PubMed1998

Effects of isoenergetic glucose-based or lipid-based parenteral nutrition on glucose metabolism, de novo lipogenesis, and respiratory gas exchanges in critically ill patients.

OBJECTIVE: To compare the effects of isocaloric, isonitrogenous carbohydrate nutrition vs. lipid-based total parenteral nutrition on respiratory gas exchange and intermediary metabolism in critically ill patients. DESIGN: Prospective, clinical trial. SETTING: Surgical intensive care unit in a major university hospital in Switzerland. PATIENTS: Sixteen patients admitted to the surgical intensive care unit. INTERVENTIONS: Patients were randomized to receive isocaloric isonitrogenous total parenteral nutrition (TPN) containing 75% (TPN-glucose) or 15% (TPN-lipid) glucose over a 5-day period. MEASUREMENTS AND MAIN RESULTS: Indirect glucose metabolism was assessed from plasma carbon-13 (13C)-labeled glucose and 13C-labeled CO2 production during a tracer infusion of uniformly 13C-labeled glucose, and de novo lipogenesis was estimated from the incorporation of 13C into palmitate-very low density lipoproteins (VLDL) during a tracer infusion of 1-(13)C acetate. Compared with TPN-lipid, TPN-glucose increased plasma glucose more (by 26% vs. 7%, p < .05), increased insulin more (by 284% vs. 40%, p < .01), and increased total CO2 more (by 15% vs. 0%, p < .01). Both nutrient mixtures failed to inhibit endogenous glucose production and net protein oxidation, suggesting absence of suppression of gluconeogenesis. Fractional de novo lipogenesis was markedly increased by TPN-glucose to 17.4% vs. 3.3% with TPN lipids. CONCLUSIONS: The rate of glucose administration commonly used during TPN of critically ill patients does not suppress endogenous glucose production or net protein loss, but markedly stimulates de novo lipogenesis and CO2 production. Increasing the proportion of fat may be beneficial, provided that lipid emulsion has no adverse effects.

Adolescent↗
PubMed1997

Energy metabolism in sepsis and injury.

The development of malnutrition is often rapid in critically ill patients with sepsis and severe trauma. In such patients, a wide array of hormonal and nonhormonal mediators are released, inducing complex metabolic changes. Hypermetabolism, associated with protein and fat catabolism, negative nitrogen balance, hyperglycemia, and resistance to insulin, constitute the hallmark of this response. Critically ill patients demonstrate a marked alteration in the adaptation to prolonged starvation: resting metabolic rate and tissue catabolism stay elevated, while ketogenesis remains suppressed. The response to nutrition support is impaired. Substrate use is modified in septic and traumatized patients. Glucose administration during severe aggression does not suppress the enhanced hepatic glucose production and the lipolysis. This phenomenon, related to tissue insulin resistance, ensures a high flow of glucose to the predominantly glucose-consuming cells, such as the wound, the inflammatory, and immune cells, all insulin-independent cells. In addition, the elevated protein catabolism is difficult to abolish, even during aggressive nutrition support. Thus, in patients with prolonged aggression, these alterations produce a progressive loss of body cell mass and foster the development of malnutrition and it dire complications. In this review, the relevant physiologic data and the nutritional implications related to energy metabolism in septic and injured patients are discussed, while potential therapeutic strategies are proposed.

Basal Metabolism↗
PubMed1997

Cytokines, nitrite/nitrate, soluble tumor necrosis factor receptors, and procalcitonin concentrations: comparisons in patients with septic shock, cardiogenic shock, and bacterial pneumonia.

OBJECTIVES: To determine and compare the respective concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, soluble TNF receptors, nitrite/nitrate (NO2-/NO3-), and procalcitonin in the plasma of patients with septic shock, cardiogenic shock, and bacterial pneumonia without shock; and to assess the predictive value of these mediators in defining patients with septic shock. DESIGN: Cohort study, comparing normal volunteers (controls) and patients with septic shock, cardiogenic shock, and bacterial pneumonia. SETTING: A collaborative study among an intensive care unit, an emergency room, and three research laboratories. PATIENTS: Mediators were measured at various times in 15 patients with septic shock (during the shock phase and during the recovery phase), in seven patients with cardiogenic shock during the shock phase, and in seven patients with severe bacterial pneumonia on day 1 of admission. INTERVENTIONS: Blood samples were collected at various times during the course of the disease. MEASUREMENTS AND MAIN RESULTS: TNF-alpha values were highest in the acute phase of septic shock (53 to 131 pg/mL during septic shock), while patients with bacterial pneumonia had intermediate concentrations (32 pg/mL). TNF-alpha concentrations were normal in patients with cardiogenic shock. IL-6 concentrations were highest in patients with acute septic shock (85 to 385 pg/mL). However, in contrast to TNF-alpha concentrations, IL-6 concentrations were normal in patients with bacterial pneumonia and increased in patients with cardiogenic shock (78 pg/mL). Soluble TNF receptors were increased in all three groups vs. controls, with the highest increase in patients with septic shock. NO2-/NO3- concentrations were highest (72 to 140 mM) in patients with septic shock, and were < 40 mM in the other groups of patients. Procalcitonin concentrations were only markedly increased in patients with septic shock (72 to 135 ng/mL, compared with approximately 1 ng/mL in the three other groups). The best predictive value for septic shock was found to be the measurements of NO2-/NO3- and procalcitonin concentrations. CONCLUSIONS: These observations showed that increase of proinflammatory cytokines was a consequence of inflammation, not of shock. In this study comparing various shock and infectious states, measurements of NO2-/NO3- concentration and procalcitonin concentration represented the most suitable tests for defining patients with septic shock.

Adult↗
PubMed1996

Relations between the selenium status and the low T3 syndrome after major trauma.

OBJECTIVE: Thyroxine (T4) is deiodinated to triiodothyronine (T3) by the hepatic type I iodothyronine deiodinase, a selenoprotein that is sensitive to selenium (Se) deficiency. After severe injury, T4 deiodination is decreased, leading to the low T3 syndrome. Injury increases free radical production, which inactivates the iodothyronine deiodinase. The aims were to study the Se status after major trauma and to investigate its relation to the low T3 syndrome. DESIGN: Preliminary prospective descriptive study. SETTING: Intensive care unit at a university teaching hospital. PATIENTS AND METHODS: 11 patients aged 41 +/- 4 years (mean +/- SEM), with severe multiple injuries (Injury Severity Score 29 +/- 2 points). A balance study was performed from day 1 to day 7. Serum and urine samples were collected from the time of admission until day 7, then on days 10, 15, 20, 25 and 30. Non-parametric tests and Pearson's correlation coefficients were used for analysis. RESULTS: Cumulated Se losses were 0.88 +/- 0.1 mumol/24h. Serum Se was decreased from admission to day 7. T3, free T3, and the T3/T4 ratio were low until day 5, being lowest on day 2; T4 and thyroid stimulating hormone were normal. Serum Se was correlated with T3 (r = 0.55, p = 0.0001), and with free T3 (r = 0.35). CONCLUSION: Se status is altered after trauma, with decreased Se serum levels upon admission to the ICU but with no major Se losses. Se is probably redistributed to the tissues. The correlation between Se and T3, along with the parallel decrease in T4 deiodination, indicates that reduced deiodination might be related to the transient decrease in serum Se.

Adult↗
PubMed1996

Effects of sodium lactate on ventilation and acid-base balance in healthy humans.

Sodium lactate inhibits ventilation when infused in healthy human subjects. This effect has been attributed to lactate-induced metabolic alkalosis. In order to further delineate the mechanisms responsible for this depression of ventilation, healthy humans were infused with sodium lactate with or without acetazolamide. Sodium lactate increased blood pH from 7.37 +/- 0.02 to 7.47 +/- 0.01 and induced a sustained urinary excretion of bicarbonate. PO2 of arterialized blood decreased by 10.3 +/- 2.1 mmHg, indicating an inhibition of ventilation. Acetazolamide decreased lactate-induced alkalinisation of blood (pH after lactate + acetazolamide 7.42 +/- 0.02), but did not prevent the drop in PO2. Acetazolamide alone tended to stimulate ventilation, as indicated by an increase in PO2. These results indicate that sodium lactate inhibits ventilation independently of changes in systemic blood pH. Alkalinization of the cerebrospinal fluid, or other central effects of lactate, is probably responsible for this ventilatory depression.

Acetazolamide↗
PubMed1995

Hypotensive effect of nimodipine during treatment for aneurysmal subarachnoid haemorrhage.

To determine the incidence of induced systemic hypotension in patients after aneurysmal subarachnoid haemorrhage (SAH) and nimodipine treatment 87 consecutive cases were reviewed. The patients were managed according to the same Nimodipine treatment protocol. After confirmation of SAH the nimodipine treatment was started as a continuous intravenous perfusion at a dosage of 0.5 mg/h and gradually increased every 6 hours if haemodynamically tolerated until the maintenance dose of 2 mg/h was reached. Median systemic pressure was continuously measured and tolerated until a lowest limit of 75 mmHg. In 31 patients (36%) hypotension with values below 75 mmHg during at least 30 minutes was noted and needed Nimodipine reduction. Intravenous Nimodipine administration was responsible for hypotension in 26 cases as compared to 5 cases due to oral administration. 38% of all patients required support by vaso-active agents (Dopamine or Nor-adrenaline). There was no statistically significant difference of incidence of delayed ischaemic deterioration comparing the Nimodipine-reduction group with the normal dose group. This study demonstrates that a considerable risk exists of Nimodipine induced hypotension in intravenous administration despite gradually increasing the doses. Correction of hypotension through further induced hypervolaemia accompanied by vasoactive agents can lead to critical haemodynamic situations. We therefore recommend oral Nimodipine administration.

Administration, Oral↗