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Objective.Current wearable respiratory monitoring devices provide a basic assessment of the breathing pattern of the examined subjects. More complex monitoring is needed for healthcare applications in patients with lung diseases. A multi-sensor vest allowing continuous lung imaging by electrical impedance tomography (EIT) and auscultation at six chest locations was developed for such advanced application. The aims of our study were to determine the vest's capacity to record the intended bio-signals, its safety and the comfort of wearing in a first clinical investigation in healthy adult subjects.Approach.Twenty subjects (age range: 23-65 years) were studied while wearing the vests during a 14-step study protocol comprising phases of quiet and deep breathing, slow and forced full expiration manoeuvres, coughing, breath-holding in seated and three horizontal postures. EIT, chest sound and accelerometer signals were streamed to a tablet using a dedicated application and uploaded to a back-end server. The subjects filled in a questionnaire on the vest properties using a Likert scale.Main results.All subjects completed the full protocol. Good to excellent EIT waveforms and functional EIT images were obtained in 89% of the subjects. Breathing pattern and posture dependent changes in ventilation distribution were properly detected by EIT. Chest sounds were recorded in all subjects. Detection of audible heart sounds was feasible in 44%-67% of the subjects, depending on the sensor location. Accelerometry correctly identified the posture in all subjects. The vests were safe and their properties positively rated, thermal and tactile properties achieved the highest scores.Significance.The functionality and safety of the studied wearable multi-sensor vest and the high level of its acceptance by the study participants were confirmed. Availability of personalized vests might further advance its performance by improving the sensor-skin contact.

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Classical approaches to make high-quality measurements of biopotential signals require the use of shielded or multi-wire cables connecting the electrodes to a central unit in a star arrangement. Consequently, increasing the number of leads increases cabling and connector complexity which is not only limiting patient comfort but also anticipated as the main limiting factor for future miniaturization and cost reduction of tomorrow's wearables. We have recently introduced a novel sensing architecture that significantly reduces cabling complexity by eliminating shielded or multi-wire cables as well as by allowing simple connectors thanks to a bus arrangement. In this architecture, electrodes are replaced by so-called cooperative sensors. However, in this design, one of the cooperative sensors needs to be equipped with two contacts with the skin for proper common mode rejection, thus making its miniaturization problematic. This paper presents a novel common mode rejection principle which overcomes this limitation. When compared to others, the suggested approach is advantageous as it keeps the cabling complexity to its minimum. First measurements demonstrated in a real-life scenario the feasibility of this common mode rejection principle for a wearable 12-lead electrocardiogram monitoring system.

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Cooperative sensors is a novel measurement architecture that allows the acquiring of biopotential signals on patients in a comfortable and easy-to-integrate manner. The novel sensors are defined as cooperative in the sense that at least two of them work in concert to measure a target physiological signal, such as a multi-lead electrocardiogram or a thoracic bioimpedance.This paper starts by analysing the state-of-the-art methods to simultaneously measure biopotential and bioimpedance signals, and justifies why currently (1) passive electrodes require the use of shielded or double-shielded cables, and (2) active electrodes require the use of multi-wired cabled technologies, when aiming at high quality physiological measurements.In order to overcome the limitations of the state-of-the-art, a new method for biopotential and bioimpedance measurement using the cooperative sensor is then presented. The novel architecture allows the acquisition of the aforementioned biosignals without the need of shielded or multi-wire cables by splitting the electronics into separate electronic sensors comprising each of two electrodes, one for voltage measurement and one for current injection. The sensors are directly in contact with the skin and connected together by only one unshielded wire. This new configuration requires one power supply per sensor and all sensors need to be synchronized together to allow them to work in concert.After presenting the working principle of the cooperative sensor architecture, this paper reports first experimental results on the use of the technology when applied to measuring multi-lead ECG signals on patients. Measurements performed on a healthy patient demonstrate the feasibility of using this novel cooperative sensor architecture to measure biopotential signals and compliance with common mode rejection specification accordingly to international standard (IEC 60601-2-47) has also been assessed.By reducing the need of using complex wiring setups, and by eliminating the presence of central recording devices (cooperative sensors directly sense and store the measured biosignals on the site), the depicted novel technology is a candidate to a novel generation of highly-integrated, comfortable and reliable technologies that measure physiological signals in real-life scenarios.

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The results of a simplified quantitative broth dilution quantitative tip culture (QTC) of 331 central venous catheters were compared with clinical data prospectively recorded in critically III patients to diagnose bacteremic or nonbacteremic catheter-related sepsis (CRS) (36 catheters), as opposed to contamination (42 catheters) or simple colonization from a distant septic focus (seven catheters). Thirty-five of 36 catheters associated with CRS yielded 10(3) colony-forming units per milliliter (CFU/mL) or more, and 3.8 X 10(2) Candida organisms grew from one. In contrast, 5 X 10(2) CFU/mL or less grew from 37 of 42 contaminated catheters. A QTC of 10(3) CFU/mL or more was 97.5% sensitive and 88% specific for the diagnosis of CRS. The QTC appeared especially useful for the diagnosis of CRS secondary to blood-borne seeding of catheters, or associated with coagulase-negative staphylococci.

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An explanation is provided of the logical steps taken before assigning patients to critical care therapy in a major multidisciplinary intensive care unit of the University of Paris at the Hospital Henri Mondor. The factors considered by the staff in deciding to terminate intensive therapy are also enumerated. This system has not been influenced by the major legal pressures found in the United States but has been shaped by more chronic fiscal constraints.

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The release of platelet-derived vasoactive substances, particularly serotonin (5-HT), have been implicated in the pulmonary vasoconstrictor response following acute pulmonary embolism. Therefore, we studied the effects of infusing ketanserin, a 5-HT blocking agent, upon pulmonary and systemic hemodynamics and gas exchange in 10 patients with severe acute pulmonary embolism. These patients evidenced 45 +/- 17% mean angiographic pulmonary vascular obstruction. Ketanserin significantly decreased the mean pulmonary arterial pressure from 26 +/- 6 to 23 +/- 5 mm Hg (p less than 0.001). The total pulmonary vascular resistance decreased from 9.1 +/- 3.2 to 8.3 +/- 2.5 mm Hg/L X min X m2 (p less than 0.001). However, the mean cardiac index was unchanged. The systemic arterial and right atrial pressures were significantly decreased after ketanserin. The PaO2 increased in all patients from 60.5 +/- 12.6 to 66.5 +/- 13.6 mm Hg (p less than 0.05), whereas the venous admixture was unchanged. This was attributed to an increased PVO2 (27 +/- 7 to 30 +/- 5 mmHg, p less than 0.01) secondary to a reduction of calculated peripheral oxygen consumption during ketanserin infusion. The results indicate ketanserin is a mild pulmonary vasodilator and can reduce the pulmonary hypertension and increase the PaO2 after pulmonary embolism.

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All patients admitted during a 33-month period to a multidisciplinary intensive care unit were prospectively studied in order to determine the incidence and severity of drug-induced illness leading to the admission. The role of underlying diseases was assessed and the avoidability of drug-induced illness considered. Out of 1651 patients, 97 (5.88%) were admitted because of drug-induced illness; 74 of these had serious underlying diseases. 13 (13.4%) of the 97 patients died, but underlying diseases accounted for 4 of the 13 fatalities. In nearly half of the cases, the drug-induced illness appeared potentially avoidable.

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A 0.01 and 0.1-mg/kg dose of iv naloxone was administered to seven patients in septic shock, in order to evaluate naloxone's hemodynamic effect and possible relation to changes in plasma beta-endorphin and catecholamine levels. Naloxone failed to modify cardiac index, blood pressure, heart rate, and systemic vascular resistance. Plasma beta-endorphin, norepinephrine, and epinephrine were elevated but did not change after naloxone administration. These results suggest that beta-endorphin release is a consequence but not a cause of shock, and that the beneficial hemodynamic effects of naloxone in animal studies could be related to species differences or nociceptive stimulations.

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Two cases of rapidly fatal Listeria rhombencephalitis with normal cerebrospinal fluid (CSF) findings occurred in previously healthy adults. The infection presented with nausea and headache followed by fever and signs of lower cranial nerve dysfunction, without associated meningismus, and progressed to death within four and six days of hospitalization. Because of normal CSF findings (including ventricular fluid in one patient) and negative culture results of both blood and CSF, the diagnosis was not suspected. Listeriosis should be considered early in any febrile patient presenting with signs of brain-stem dysfunction, even if CSF findings are normal.

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Pulmonary complications of lymphography are usually described as radiological infiltrates without clinical symptoms. However, a case is here reported of an adult respiratory distress syndrome occurring after lymphography in a 60 year old female lymphoma patient. Pulmonary oedema developed within 48 h; haemodynamic study showed a normal capillary wedge pressure. The patient died from intractable low cardiac output within 24 h. Post-mortem examination showed pulmonary lymphocytic infiltration and multiple fat emboli. The lack of lymphatic drainage was probably responsible for the intravascular passage of lipid-soluble contrast medium, this giving endothelial lesions. In such patients with preexisting lung disease or pulmonary involvement in haematological disease, lymphography has to be considered carefully.

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Delayed-onset pulmonary edema complicating severe diabetic ketoacidosis was observed twice in one patient. Hemodynamic measurements during the second episode showed normal transmural pulmonary capillary wedge pressure, suggesting an alteration in alveolocapillary permeability. Hyperventilation and acidosis may underlie this alteration. Vigorous fluid therapy, while decreasing oncotic pressure, may also contribute to the pulmonary edema. The two episodes in one patient suggest that pulmonary microvascular diabetic angiopathy may predispose some diabetics with severe ketoacidosis to increased-permeability pulmonary edema.

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A prospective study was undertaken in a multidisciplinary intensive care unit to determine the proportion of complications due to anticoagulant therapy, to evaluate their severity and to estimate what proportion was potentially avoidable. Among 1911 hospitalized patients over a 3 year period, 30 patients had a complication of anticoagulant therapy (1,57 p. 100). The causality was definite in 14 cases, probable in 14 and possible in 2 cases. Nineteen p. 100 were hemorrhagic complications. These iatrogenic illnesses were fatal in 5 cases, life-threatening in 6, moderate in 15 and minor in 4 cases. Potentially avoidable complications accounted for 60 p. 100 of the cases and were due to biological overdosage or interaction between drugs. Our results indicate that some complications of anticoagulant therapy could be reduced or eliminated by medical education and increased information.

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Plasma levels of norepinephrine (NE), epinephrine (E), immunoreactive insulin (IRI), and glucose were measured in six healthy volunteers after glucose consumption and in six volunteers after a water solution. Ingestion of the glucose (100 g) solution significantly decreased E levels from 46.7 +/- 8.0 to 20.8 +/- 1.9 pg/mL (P less than 0.01). Three hours after the glucose ingestion, plasma E levels nearly returned to basal values. Plasma IRI and glucose levels peaked at 45 minutes after glucose consumption (P less than 0.01), then declined toward basal values. Plasma NE levels were unaffected by glucose consumption. There were no changes in glucose, IRI, NE, or E levels in the control group. These results suggest that E behaves as a counter-regulatory hormone to insulin under stimulation by glucose.

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The influence of increased enteral caloric intakes on respiratory gas exchanges was evaluated in 6 patients (5 men, 1 woman; mean-age: 54 years) in steady state and requiring continuous ventilatory support. Oxygen consumption (VO2), carbon dioxide production (VCO2), respiratory quotient (R), determined using an open circuit indirect calorimetric method, and arterial blood gases were measured on two consecutive days while ventilation conditions were unchanged. On the first day, the patients received a water diet only and on the following day an enteral caloric load (1491 +/- 65 Kcal/m2/24 h). The results showed a significant increase in VO2 (p less than 0.05) and R (p less than 0.001) and a rise in VCO2 from 106 +/- 4 to 139 +/- 9 ml/mn/m2 (p less than 0.01). The rise in VCO2 induced an increase of arterial carbon dioxide tension (PaCO2) from 26.3 +/- 1.6 to 34.4 +/- 2.4 mmHg (p less than 0.001). This study showed that because of the constancy of alveolar ventilation, the enteral nutrition-related increase of VCO2 is responsible for a PaCO2 increase and emphasized the need for adjusting artificial ventilation to any change in caloric intake in patients supported with mechanical ventilation.

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Three cases of splenic infarction complicated by abscess formation during bacterial endocarditis are reported. In all three cases there were associated clinical abdominal signs and, in one case, there was persistently positive hemocultures. The diagnosis was made by CAT scanning. The three patients underwent splenectomy and one patient also underwent valve replacement the same day. The methods of early diagnosis of splenic complications during endocarditis and the indications of splenectomy are discussed. Ultrasonography and abdominal CAT scanning are the most sensitive diagnostic methods for splenic lesions. As splenic rupture is associated with a high mortality and this complication may occur at any time during infarction complicated by abscess formation, early splenectomy is justified when abdominal clinical signs are elicited associated with a persistent, infectious syndrome with or without positive blood cultures, under appropriate antibiotic therapy. Splenectomy should also be considered if valve replacement is carried out in the same circumstances to avoid infection of the prosthesis.

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