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Biomedical subjects

L Gallart

Publications and source records attributed to L Gallart.

At least 19 recordsLinked to original sources
PubMed2003

Simple method to determine the size of the laryngeal mask airway in children.

BACKGROUND AND OBJECTIVE: The size of the laryngeal mask airway in children is determined by the patient's weight. However, in some instances an alternative method may be wanted. The aim was to search for a new method that would be easy to perform at the bedside. METHODS: The size of the laryngeal mask airway was determined in 183 children by choosing the laryngeal mask that best matched the combined widths of the patient's index, middle and ring fingers. The results were compared with the standard method recommended by the manufacturer's weight-related guidelines. The patients were classified in different groups depending on the laryngeal mask airway sizes determined by both methods. A kappa coefficient evaluated the agreement between both techniques. RESULTS: The kappa coefficient was 0.81, showing an 'excellent agreement' between both methods. The size was the same for both methods in 142 children (78%). The disagreement between both techniques was only of one size in the remaining 41 patients (22%). In such patients, the weight was a borderline value that would indicate a change in the size of the laryngeal mask airway using the classic method. CONCLUSIONS: This new approach is of valid and practical use in children, particularly as an alternative in those situations where the patient's weight is unknown, such as in emergency situations or in those borderline instances where an alternative measurement would be useful.

Adolescent↗
PubMed1999

Molecular pathology of multiple endocrine neoplasia type I: two novel germline mutations and updated classification of mutations affecting MEN1 gene.

Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder characterized by the combined development of tumors in several endocrine glands and other tissues. The MEN1 gene was recently identified and isolated by positional cloning. This gene was screened in two unrelated MEN1 Spanish kindreds (with four affected members and seven asymptomatic members) using single-strand conformation polymorphism, DNA sequencing, and restriction enzyme analysis. Two novel germline mutations were identified: a missense in exon 2 (H139R) and a splice-site in intron 9 (1461-2A>C). These findings allowed us to identify the MEN1 carriers among the seven asymptomatic members analyzed. An updated review of the mutations and polymorphisms found in the analysis of the MEN1 gene is provided. The report of all germline mutations causing MEN1 and easy access to this updated information are both of special diagnostic interest, because this greatly facilitates the task of attributing the disorder to a specific mutation found in a given MEN1 family. This is especially helpful in the critical differentiation of missense mutations from nonsynonymous polymorphisms that fit the pattern of segregation of the disease, but do not cause it.

Adolescent↗
PubMed1998

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.

Administration, Oral↗
PubMed1998

Intravenous almitrine combined with inhaled nitric oxide for acute respiratory distress syndrome. The NO Almitrine Study Group.

Inhaled nitric oxide (iNO), a selective pulmonary vasodilator and intravenously administered almitrine, a selective pulmonary vasoconstrictor, have been shown to increase PaO2 in patients with acute respiratory distress syndrome (ARDS). This prospective study was undertaken to assess the cardiopulmonary effects of combining both drugs. In 48 consecutive patients with early ARDS, cardiorespiratory parameters were measured at control, after iNO 5 ppm, after almitrine 4 micrograms. kg-1. min-1, and after the combination of both drugs. In 30 patients, dose response to 2, 4, and 16 micrograms. kg-1. min-1 of almitrine with and without NO was determined. Almitrine and lactate plasma concentrations were measured in 17 patients. Using pure O2, PaO2 increased by 75 +/- 8 mm Hg after iNO, by 101 +/- 12 mm Hg after almitrine 4 micrograms. kg-1. min-1, and by 175 +/- 18 mm Hg after almitrine combined with iNO (p < 0.001). In 63% of the patients, PaO2 increased by more than 100% with the combination of both drugs. Mean pulmonary artery pressure (Ppa) increased by 1.4 +/- 0.2 mm Hg with almitrine 4 micrograms/kg/ min (p < 0.001) and decreased by 3.4 +/- 0.4 mm Hg with iNO and by 1.5 +/- 0.3 mm Hg with the combination (p < 0.001). The maximum increase in PaO2 was obtained at almitrine concentrations <= 4 micrograms. kg-1. min-1, whereas almitrine increased Ppa dose-dependently. Almitrine plasma concentrations also increased dose-dependently and returned to values close to zero after 12 h. In many patients with early ARDS, the combination of iNO 5 ppm and almitrine 4 micrograms. kg-1. min-1 dramatically increases PaO2 without apparent deleterious effect allowing a rapid reduction in inspired fraction of O2. The long-term consequences of this immediate beneficial effect remain to be determined.

Administration, Inhalation↗
PubMed1997

Distribution of inhaled nitric oxide during sequential and continuous administration into the inspiratory limb of the ventilator.

OBJECTIVES: The concentrations of nitric oxide (NO) in the ventilatory circuits and the patient's airways were compared between sequential (SQA) and continuous (CTA) administration during inspiratory limb delivery. DESIGN: Prospective controlled study. SETTING: 14-bed Surgical Intensive Care Unit of a teaching University hospital. PATIENTS AND PARTICIPANTS: Eleven patients with acute lung injury on mechanical ventilation and two healthy volunteers. INTERVENTIONS: A prototype NO delivery device (Opti-NO) and César ventilator were set up in order to deliver 1, 3 and 6 parts per million (ppm) of NO into the bellows of a lung model in SQA and CTA. Using identical ventilatory and Opti-NO settings, NO was administered to the patients with acute lung injury. MEASUREMENTS AND RESULTS: NO concentrations measured from the inspiratory limb [INSP-NOMeas] and the trachea [TRACH-NOMeas] using fast response chemiluminescence were compared between the lung model and the patients using controlled mechanical ventilation with a constant inspiratory flow. INSP-NOMeas were stable during SQA and fluctuated widely during CTA (fluctuation at 6 ppm = 61% in the lung model and 58 +/- 3% in patients). In patients, [TRACH-NOMeas] fluctuated widely during both modes (fluctuation at 6 ppm = 55 +/- 3% during SQA and 54 +/- 5% during CTA). The NO flow requirement was significantly lower during SQA than during CTA (74 +/- 0.5 vs 158 +/- 2.2 ml.min-1 to attain 6 ppm, p = 0.0001). INSP-NOMeas were close to the values predicted using a classical formula only during SQA (bias = -0.1 ppm, precision = +/-1 ppm during SQA; bias = 2.93 ppm and precision = +/-3.54 ppm during CTA). During SQA, INSP-NOMeas varied widely in healthy volunteers on pressure support ventilation. CONCLUSIONS: CTA did not provide homogenous mixing of NO with the tidal volume and resulted in fluctuating INSP-NOMeas. In contrast, SQA delivered stable and predictable NO concentrations during controlled mechanical ventilation with a constant inspiratory flow and was economical compared to CTA. However, SQA did not provide stable and predictable NO concentrations during pressure support ventilation.

Analysis of Variance↗
PubMed1997

Permissive hypercapnia with and without expiratory washout in patients with severe acute respiratory distress syndrome.

BACKGROUND: Permissive hypercapnia is a ventilatory strategy aimed at avoiding lung volutrauma in patients with severe acute respiratory distress syndrome (ARDS). Expiratory washout (EWO) is a modality of tracheal gas insufflation that enhances carbon dioxide removal during mechanical ventilation by reducing dead space. The goal of this prospective study was to determine the efficacy of EWO in reducing the partial pressure of carbon dioxide (PaCO2) in patients with severe ARDS treated using permissive hypercapnia. METHODS: Seven critically ill patients with severe ARDS (lung injury severity score, 3.1 +/- 0.3) and no contraindications for permissive hypercapnia were studied. On the first day, hemodynamic and respiratory parameters were measured and the extent of lung hyperdensities was assessed using computed tomography. A positive end-expiratory pressure equal to the opening pressure identified on the pressure-volume curve was applied. Tidal volume was reduced until a plateau airway pressure of 25 cm H2O was reached. On the second day, after implementation of permissive hypercapnia, EWO was instituted at a flow of 15 l/min administered during the entire expiratory phase into the trachea through the proximal channel of an endotracheal tube using a ventilator equipped with a special flow generator. Cardiorespiratory parameters were studied under three conditions: permissive hypercapnia, permissive hypercapnia with EWO, and permissive hypercapnia. RESULTS: During permissive hypercapnia, EWO decreased PaCO2 from 76 +/- 4 mmHg to 53 +/- 3 mmHg (-30%; P < 0.0001), increased pH from 7.20 +/- 0.03 to 7.34 +/- 0.04 (P < 0.0001), and increased PaO2 from 205 +/- 28 to 296 +/- 38 mmHg (P < 0.05). The reduction in PaCO2 was accompanied by an increase in end-inspiratory plateau pressure from 26 +/- 1 to 32 +/- 2 cm H2O (P = 0.001). Expiratory washout also decreased cardiac index from 4.6 +/- 0.4 to 3.7 +/- 0.3 l.min-1.m-2 (P < 0.01), mean pulmonary arterial pressure from 28 +/- 2 to 25 +/- 2 mmHg (P < 0.01), and true pulmonary shunt from 47 +/- 2 to 36 +/- 3% (P < 0.01). CONCLUSIONS: Expiratory washout is an effective and easy-to-use ventilatory modality to reduce PaCO2 and increase pH during permissive hypercapnia. However, it significantly increases airway pressures and lung volume through expiratory flow limitation, reexposing some patients to a risk of lung volutrauma if the extrinsic positive end-expiratory pressure is not substantially reduced.

Acute Disease↗
PubMed1997

Factors influencing the tracheal fluctuation of inhaled nitric oxide in patients with acute lung injury.

BACKGROUND: Inhaled nitric oxide (NO) improves arterial oxygenation in patients with acute lung injury (ALI) by selectively dilating pulmonary vessels perfusing ventilated lung areas. It can be hypothesized that NO uptake from the lung decreases with increasing ventilation perfusion mismatch. This study was undertaken to determine the factors influencing the fluctuation of tracheal NO concentration over the respiratory cycle as an index of NO pulmonary uptake in patients with ALI. METHODS: By using a prototype system (Opti-NO) delivering a constant flow of NO only during the inspiratory phase, 3 and 6 ppm of NO were administered during controlled mechanical ventilation into a lung model and to 11 patients with ALI. All patients had a thoracic computed tomography (CT) scan. Based on an analysis of tomographic densities, lungs were divided into three zones: normally aerated (-1.000 to -500 Hounsfield units [HU]), poorly aerated (-500 to -100 HU), and nonaerated (-100 to +100 HU), and the volume of each zone was computed. Concentrations of NO in the inspiratory limb and trachea were continuously measured by a fast-response chemiluminescence apparatus. RESULTS: In the lung model, tracheal NO concentration was stable with minor fluctuation. In contrast, in patients, tracheal NO concentration fluctuated widely during the respiratory cycle (55 +/- 10%). Because uptake of NO from the lungs was absent in the lung model but present in the patients, this fluctuation was considered as an index of pulmonary uptake of NO. This was further substantiated by (1) the coincidence of the peak and minimum tracheal NO concentration with the end-inspiratory and end-expiratory phases, respectively, and (2) continued decrease of tracheal NO concentration during prolonged expiratory phase. In patients with ALI, the fluctuation of tracheal NO concentration expressed as the difference between inspiratory and expiratory NO concentrations divided by inspiratory NO concentration was greater at 6 ppm than at 3 ppm (P < 0.01), was linearly correlated with normally aerated lung volume, inversely correlated with alveolar dead space and with poorly aerated lung volume. CONCLUSION: In patients with ALI, fluctuation of tracheal NO concentration over the respiratory cycle can be considered as an index of NO uptake from the lungs that depends on aerated lung volume and perfusion of ventilated lung areas. At bedside, it may be used to follow the evolution of ventilation-perfusion mismatch.

Administration, Inhalation↗
PubMed1997

Inhaled nitric oxide in acute respiratory distress syndrome with and without septic shock requiring norepinephrine administration: a dose-response study.

BACKGROUND: The aim of this prospective study was to assess whether the presence of septic shock could influence the dose response to inhaled nitric oxide (NO) in NO-responding patients with adult respiratory distress syndrome (ARDS). RESULTS: Eight patients with ARDS and without septic shock (PaO2 = 95 +/- 16 mmHg, PEEP = 0, FiO2 = 1.0), and eight patients with ARDS and septic shock (PaO2 = 88 +/- 11 mmHg, PEEP = 0, FiO2 = 1.0) receiving exclusively norepinephrine were studied. All responded to 15 ppm inhaled NO with an increase in PaO2 of at least 40 mmHg, at FiO2 1.0 and PEEP 10 cmH2O. Inspiratory intratracheal NO concentrations were recorded continuously using a fast response time chemiluminescence apparatus. Seven inspiratory NO concentrations were randomly administered: 0.15, 0.45, 1.5, 4.5, 15, 45 and 150 ppm. In both groups, NO induced a dose-dependent decrease in mean pulmonary artery pressure (MPAP), pulmonary vascular resistance index (PVRI), and venous admixture (QVA/QT), and a dose-dependent increase in PaO2/FiO2 (P </= 0.012). Dose-response of MPAP and PVRI were similar in both groups with a plateau effect at 4.5 ppm. Dose-response of PaO2/FiO2 was influenced by the presence of septic shock. No plateau effect was observed in patients with septic shock and PaO2/FiO2 increased by 173 +/- 37% at 150 ppm. In patients without septic shock, an 82 +/- 26% increase in PaO2/FiO2was observed with a plateau effect obtained at 15 ppm. In both groups, dose-response curves demonstrated a marked interindividual variability and in five patients pulmonary vascular effect and improvement in arterial oxygenation were dissociated. CONCLUSION: For similar NOinduced decreases in MPAP and PVRI in both groups, the increase in arterial oxygenation was more marked in patients with septic shock.

Journal Article↗
PubMed1996

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.

Adult↗
PubMed1995

Effects of interpleural bupivacaine on respiratory muscle strength and pulmonary function.

BACKGROUND: Several reports suggest that interpleural local anesthetics may have deleterious effects on respiratory function. The current study investigated the effects of interpleural bupivacaine on human respiratory muscles and lung function. METHODS: Thirteen patients (55 +/- 4 yr old) with normal respiratory function and scheduled for cholecystectomy entered the study before surgery. Respiratory parameters were compared before and after the interpleural administration of 20 ml 0.5% bupivacaine plus 1:200,000 epinephrine while patients were supine; we evaluated breathing pattern, dynamic and static lung volumes, airway conductance, maximal inspiratory pressures (at the mouth; at the esophagus [Pessniff]; at the abdomen [Pgasniff]; and transdiaphragmatic [Pdisniff]), functional reserve (tension-time index) of the diaphragm, and maximal expiratory pressures (at the mouth; at the esophagus [Pescough]; and at the abdomen [Pgacough]). Hemoglobin oxygen saturation by pulse oximetry, heart rate, and mean arterial pressure were continuously monitored. RESULTS: Respiratory rate (15 +/- 1 to 19 +/- 1 breaths/min; P < 0.01) and heart rate (78 +/- 3 to 83 +/- 3 beats/min; P < 0.01) were slightly increased. Dynamic and static lung volumes, airway conductance, hemoglobin saturation, and the remaining breathing pattern parameters were unchanged. Regarding respiratory muscles, maximal inspiratory pressure at the mouth, Pessniff, and tension-time index of the diaphragm did not change. Pdisniff decreased slightly (102 +/- 10 to 92 +/- 10 cmH2O; P < 0.05) because of a change in Pgasniff (24.2 +/- 7.4 to 18.4 +/- 6.8 cmH2O; P < 0.05). Maximal expiratory pressure at the mouth remained unaltered, but Pgacough decreased (108 +/- 10 to 92 +/- 8 cmH2O; P < 0.01), and Pescough showed a trend to decrease (92 +/- 13 to 78 +/- 10 cmH2O; P = 0.074). CONCLUSIONS: In our experimental conditions, interpleural bupivacaine did not significantly change lung function or inspiratory muscle strength but induced a slight decrease in abdominal muscle strength. Although this effect was minimal, its clinical relevance needs to be evaluated further in patients with impaired respiratory function.

Adult↗
PubMedDate not supplied

A novel germline mutation in exon 5 of the multiple endocrine neoplasia type 1 gene.

The autosomal dominant multiple endocrine neoplasia type 1 (MEN1) syndrome is characterized by neoplasia of parathyroids, anterior pituitary, and gastrointestinal and pancreatic neuroendocrine tissues. Recently the gene responsible for the MEN1 syndrome has been identified on chromosome region 11q13. Most of the described mutations are nucleotide substitutions and small deletions affecting exons 2 and 3, causing protein truncation. Only one mutation in exon 5 has been found, and this corresponds to a MEN1 sporadic case. Small insertions are also rare. We studied a MENI family composed of five members, two of whom were clinically affected. We found a new germline 1 basepair insertional mutation affecting the exon 5 of the MEN1 gene in the two members affected in this MEN1 family.

Adult↗
PubMedDate not supplied

Genetic, clinical, and biochemical analysis of unrelated Spanish families with multiple endocrine neoplasia type I.

OBJECTIVE: (1) To study seven unrelated Spanish families with multiple endocrine neoplasia type I (MEN I), describing clinical features and investigating the presence of germline mutations in the MEN1 gene, and (2) to establish reference values for pancreatic polypeptide and gastrin after a standardized test meal in a healthy control group, analyzing the usefulness of this test for detecting neuroendocrine gastroenteropancreatic tumors in subjects with MEN I. METHODS: Two or three generations of 7 kindreds with MEN I, consisting of a total of 39 individual family members, were investigated. Three of the families were subjected only to genetic analysis, and the other four families were also assessed clinically. A group of 23 healthy control subjects were also studied. RESULTS: Mutations in the MEN1 gene were found in six of the seven families studied. Of the 4 families studied clinically, 12 family members were genetically affected. In these study subjects, hyperparathyroidism, adrenal adenomas, neuroendocrine gastroenteropancreatic tumors, and pituitary adenomas developed in 100%, 50%, 16%, and 12%, respectively. All demonstrated pancreatic tumors were associated with abnormal results after a test meal, but 75% of them also showed high basal hormonal measurements. CONCLUSION: Analysis of the MEN1 gene decreases the total number of subjects who need to undergo repeated clinical and biochemical studies, but genetic mutations are not detected in all families with MEN I. Hyperparathyroidism is the most common manifestation of the syndrome, but the presence of adrenal adenomas has probably been underestimated. Ingestion of a standardized test meal for stimulation of gastrin and pancreatic polypeptide could be a complementary procedure for diagnosing gastroenteropancreatic tumors in selected patients with MEN I in whom basal gastrin and pancreatic polypeptide levels are normal.

Adenoma↗
PubMedDate not supplied

[Ineffectiveness of arterial pressure measurement and cardiac rate in detecting hypoxemia in the postanesthetic period].

The purpose of the study was to analyze the hemodynamic response to hypoxemia induced during the first postoperative hour. We studied 151 patients who underwent general anesthesia for elective surgery. Arterial saturation of oxyhemoglobin (SpO2), heart rate (HR), and systolic arterial pressure (SAP) during respiration with atmospheric air were measured 20 min and 80 min after admission at the recovery room. We compared HR and SAP between hypoxemic (SpO2 less than or equal to 90%) and non-hypoxemic patients (SpO2 greater than 90%) and we did not find significant differences. SpO2 failed to correlate with HR or with SAP in any of the time samples. This lack of correlation was also observed between patients with or without halogenated anesthetic treatment. Our results indicate that the possible inhibitory effect of anesthesia on hemodynamic response to hypoxemia lasts at least during the first postoperative hour and it does not depend on the administration of halogenated anesthetics. We also conclude that postoperative hemodynamic stability is not an accurate index of the status of arterial oxygenation.

Adult↗