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Background: Intravenous fluid administration is an essential part of perioperative care for children receiving a kidney transplant. There is a paucity of evidence to guide optimal perioperative fluid management. This study aimed to identify the volume of perioperative fluids administered across 5 UK paediatric kidney transplant centres and explore associations between fluid volume administered, graft function, and fluid-related adverse events. Methods: Data were collected from five UK paediatric kidney transplant centres on perioperative fluid volumes administered, and incidence of pulmonary oedema, systemic hypertension, and requirement for intensive care support. Children < 18 years of age who received a kidney-only transplant between 1st January 2020 and 31st December 2021 were included. Results: Complete data from 102 children were analysed. The median total volume of fluid administered in 72 h was 377 ml/kg (IQR 149 ml/kg) with a high degree of variability. A negative relationship between total fluid volume administered and day 7 eGFR was noted (p < 0.001). Association between urine volume post-transplant and day 7 eGFR was also negative (p < 0.001). Adverse events were frequent but no significant difference was found in the fluid volume administered to those who developed an adverse event, vs those who did not. Conclusions: This study describes a high degree of variability in perioperative fluid volumes administered to children receiving kidney transplants. Both fluid volume and urine output were negatively associated with short-term graft function. These data contrast traditional interpretation of high urine output as a marker of graft health, and highlight the need for prospective clinical trials to optimise perioperative fluid administration for this group. A higher resolution version of the Graphical abstract is available as Supplementary information [ABSTRACT FROM AUTHOR]

B-lines in lung ultrasound (LU) are non-specific but highly informative sign of interstitial pulmonary oedema (iPE). Sustained exposure to a high-volume left-to-right patent ductus arteriosus (PDA) shunt is associated with iPE. Cardiorespiratory deterioration, named post-ligation cardiac syndrome (PLCS), may follow surgical ligation between 6 and 12 h post-operatively. We conducted a pilot longitudinal evaluation of peri-procedural LU score change. Infants < 32-week gestational age or < 1500-g birthweight undergoing PDA ligation, where pre-, 1 h and 6–12 h LU were performed, were included. Two independent raters evaluated LU score (LUS). Neonatologist performed echocardiography (NPE) was performed concurrently to appraise changes in left ventricular output (LVO). Milrinone was initiated if LVO was < 200 mL/kg/min 1 h after surgery, to prevent PLCS. The primary outcome was peri-procedural LUS change. Secondary outcomes included PLCS. Five infants were included (birthweight 787(88) g; gestational age 25.6(0.7) weeks). Postnatal age and weight at the intervention were 41(14) days and 1175(295) g. All infants, but one, received milrinone prophylaxis. None of the patients developed PLCS or required rescue HFOV. Post-interventional LUS were lower compared to pre-operative LUS (p = 0.041 vs 1 h, p = 0.042 vs 6–12 h). A concurrent fall post-operative LVO was noted (p < 0.05 vs pre-operative). Conclusion: A sustained fall in LUS after PDA ligation was identified, which most likely reflects reduction in pulmonary blood flow and interstitial edema. Changes in LUS paralleled changes in LVO, suggesting physiologic linkage. These data suggest that LU may be a useful tool to guide monitoring the biologic nature of pulmonary disease after PDA ligation. What is Known: • Sustained exposure to a high-volume left-to-right patent ductus arteriosus (PDA) shunt is associated with interstitial pulmonary oedema. • In the most immature patients, cardiorespiratory deterioration, named post-ligation cardiac syndrome, presents 6–12 h post-operatively. What is New: • An early and sustained fall in lung ultrasound score (LUS) after PDA ligation most likely reflects reduction in pulmonary blood flow and interstitial oedema. LUS changes parallel changes in left ventricular output, suggesting linkage. • LU is a promising adjunctive tool in the post-operative management of PDA ligation. [ABSTRACT FROM AUTHOR]

Background: Cardiogenic pulmonary oedema (CPE) may contribute to ventilator-associated lung injury (VALI) in patients with cardiogenic shock. The appropriate ventilatory strategy remains unclear. We aimed to evaluate the impact of ultra-low tidal volume ventilation with tidal volume of 3 ml/kg predicted body weight (PBW) in patients with CPE and veno–arterial extracorporeal membrane oxygenation (V–A ECMO) on lung inflammation compared to conventional ventilation. Methods: A single-centre randomized crossover trial was performed in the Cardiac Intensive Care Unit (ICU) at a tertiary university hospital. Seventeen adults requiring V–A ECMO and mechanical ventilation due to cardiogenic shock were included from February 2017 to December 2018. Patients were ventilated for two consecutive periods of 24 h with tidal volumes of 6 and 3 ml/kg of PBW, respectively, applied in random order. Primary outcome was the change in proinflammatory mediators in bronchoalveolar lavage fluid (BALF) between both ventilatory strategies. Results: Ventilation with 3 ml/kg PBW yielded lower driving pressures and end-expiratory lung volumes. Overall, there were no differences in BALF cytokines. Post hoc analyses revealed that patients with high baseline levels of IL-6 showed statistically significant lower levels of IL-6 and IL-8 during ultra-low tidal volume ventilation. This reduction was significantly proportional to the decrease in driving pressure. In contrast, those with lower IL-6 baseline levels showed a significant increase in these biomarkers. Conclusions: Ultra-low tidal volume ventilation in patients with CPE and V–A ECMO may attenuate inflammation in selected cases. VALI may be driven by an interaction between the individual proinflammatory profile and the mechanical load overimposed by the ventilator. Trial registration The trial was registered in ClinicalTrials.gov (identifier NCT03041428, Registration date: 2nd February 2017). [ABSTRACT FROM AUTHOR]

Background: Diaphragm dysfunction and weaning-induced pulmonary oedema are commonly involved during weaning failure, but their physiological interactions have been poorly reported. Our hypothesis was that diaphragm dysfunction is not particularly associated with weaning-induced pulmonary oedema. Methods: It was a single-centre and physiological study conducted in patients who had failed a first spontaneous breathing trial and who underwent a second trial. The diaphragm function was evaluated by measuring the tracheal pressure generated in response to a bilateral magnetic phrenic nerves stimulations. Weaning-induced pulmonary oedema was diagnosed in case of failure of the spontaneous breathing trial if patients exhibited signs of plasma concentration or echocardiographic diagnosis of pulmonary artery occlusion pressure elevation. Results: Fifty-three patients were included and 31/53 (58%) failed the spontaneous breathing trial, including 24/31 (77%) patients with weaning-induced pulmonary oedema. Diaphragm dysfunction was present in 33/53 (62%) patients. Diaphragm dysfunction or weaning-induced pulmonary oedema were present in 26/31 (84%) of the patients who failed the spontaneous breathing trial. Weaning-induced pulmonary oedema occurred in 20/33 (61%) patients with a diaphragm dysfunction and in 4/20 (20%) patients without (p = 0.005). Conclusion: Weaning-induced pulmonary oedema was three times more frequent in case of diaphragm dysfunction. Even in case of diaphragm dysfunction, physicians might be encouraged to investigate the presence of weaning-induced pulmonary oedema during weaning failure. [ABSTRACT FROM AUTHOR]

Purpose: It has been suggested that, by recruiting lung regions and enlarging the distribution volume of the cold indicator, increasing the positive end-expiratory pressure (PEEP) may lead to an artefactual overestimation of extravascular lung water (EVLW) by transpulmonary thermodilution (TPTD). Methods: In 60 ARDS patients, we measured EVLW (PiCCO2 device) at a PEEP level set to reach a plateau pressure of 30 cmH2O (HighPEEPstart) and 15 and 45 min after decreasing PEEP to 5 cmH2O (LowPEEP15′ and LowPEEP45′, respectively). Then, we increased PEEP back to the baseline level (HighPEEPend). Between HighPEEPstart and LowPEEP15′, we estimated the degree of lung derecruitment either by measuring changes in the compliance of the respiratory system (Crs) in the whole population, or by measuring the lung derecruited volume in 30 patients. We defined patients with a large derecruitment from the other ones as patients in whom the Crs changes and the measured derecruited volume were larger than the median of these variables observed in the whole population. Results: Reducing PEEP from HighPEEPstart (14 ± 2 cmH2O) to LowPEEP15′ significantly decreased EVLW from 20 ± 4 to 18 ± 4 mL/kg, central venous pressure (CVP) from 15 ± 4 to 12 ± 4 mmHg, the arterial oxygen tension over inspired oxygen fraction (PaO2/FiO2) ratio from 184 ± 76 to 150 ± 69 mmHg and lung volume by 144 [68–420] mL. The EVLW decrease was similar in "large derecruiters" and the other patients. When PEEP was re-increased to HighPEEPend, CVP, PaO2/FiO2 and EVLW significantly re-increased. At linear mixed effect model, EVLW changes were significantly determined only by changes in PEEP and CVP (p < 0.001 and p = 0.03, respectively, n = 60). When the same analysis was performed by estimating recruitment according to lung volume changes (n = 30), CVP remained significantly associated to the changes in EVLW (p < 0.001). Conclusions: In ARDS patients, changing the PEEP level induced parallel, small and reversible changes in EVLW. These changes were not due to an artefact of the TPTD technique and were likely due to the PEEP-induced changes in CVP, which is the backward pressure of the lung lymphatic drainage. Trial registration ID RCB: 2015-A01654-45. Registered 23 October 2015 [ABSTRACT FROM AUTHOR]

Background: Emergency medical services (EMS) practitioners in Ireland have been recently licensed to use continuous positive airway pressure (CPAP) ventilation for patients with pulmonary oedema. Both the British Thoracic Society and the Canadian Medical Association advocate the use of CPAP in hospital for patients with severe exacerbations of pulmonary oedema. Aims: The aim of this study was to identify prehospital patients in the Midwest, over a 6-month period, which could potentially benefit from CPAP if it were available in the National Ambulance Service. Methods: Potential CPAP patients were identified in the Advanced Paramedic Clinical Activity Study (APCAS) database and then followed up in the receiving hospital emergency department (ED) and medical records. Prior to this study, Irish guidance for prehospital use of CPAP did not exist and therefore the database was interrogated using a Toronto EMS Medical Directive. Descriptive analysis was conducted in Microsoft Excel and SPSS. Results: Emergency AS1 calls (999/112) were assessed ( n = 1369) and 141 patients (10.3, 95 % confidence interval 8.9-12.1 %) were identified as potential candidates for prehospital CPAP. Further investigation of ED records for 63 potential candidates found 36.5 % (95 % confidence interval 26-49 %) met the Toronto EMS criteria for CPAP. Conclusions: This study suggests that a suitable patient cohort for CPAP exists in the prehospital environment and highlights the need for a prospective study of CPAP use on these patients. [ABSTRACT FROM AUTHOR]

Purpose: Continuous positive airway pressure (CPAP) is a useful treatment for patients with acute cardiogenic pulmonary oedema (CPE). However, its usefulness in the out-of-hospital setting has been poorly investigated and only by small and single-centre studies. We designed a multicentre randomised study to assess the benefit of CPAP initiated out of hospital. Methods: A total of 207 patients with CPE were randomly allocated by emergency mobile medical units to receive either standard treatment alone or standard treatment plus CPAP. CPAP was maintained after admission to the intensive care unit (ICU). Inclusion criteria were orthopnoea, respiratory rate greater than 25 breaths/min, pulse oximetry less than 90% in room air and diffuse crackles. The primary end point was assessed during the first 48 h and combined: death, presence of intubation criteria, persistence of either all inclusion criteria or circulatory failure at the second hour or their reappearance before 48 h. Absence of all criteria defined successful treatment. Results: CPAP was used for 60 min [40, 65] (median [Q1, Q3]) in the pre-hospital setting and 120 min [60, 242] in ICU and was well tolerated in all patients. Treatment was successful in 79% of patients in the CPAP group and 63% in the control group ( p = 0.01), especially for persistence of inclusion criteria after 2 h (12 vs. 26%) and for intubation criteria (4 vs. 14%). CPAP was beneficial irrespective of the initial PaCO or left ventricular ejection fraction. Conclusion: Immediate use of CPAP in out-of-hospital treatment of CPE and until CPE resolves after admission significantly improves early outcome compared with medical treatment alone. [ABSTRACT FROM AUTHOR]

Impairment of lung liquid absorption can lead to severe respiratory symptoms, such as those observed in pulmonary oedema. In the adult lung, liquid absorption is driven by cation transport through two pathways: a well-established amiloride-sensitive Na channel (ENaC) and, more controversially, an amiloride-insensitive channel that may belong to the cyclic nucleotide-gated (CNG) channel family. Here, we show robust CNGA1 (but not CNGA2 or CNGA3) channel expression principally in rat alveolar type I cells; CNGA3 was expressed in ciliated airway epithelial cells. Using a rat in situ lung liquid clearance assay, CNG channel activation with 1 mM 8Br-cGMP resulted in an approximate 1.8-fold stimulation of lung liquid absorption. There was no stimulation by 8Br-cGMP when applied in the presence of either 100 μM l- cis-diltiazem or 100 nM pseudechetoxin (PsTx), a specific inhibitor of CNGA1 channels. Channel specificity of PsTx and amiloride was confirmed by patch clamp experiments showing that CNGA1 channels in HEK 293 cells were not inhibited by 100 μM amiloride and that recombinant αβγ-ENaC were not inhibited by 100 nM PsTx. Importantly, 8Br-cGMP stimulated lung liquid absorption in situ, even in the presence of 50 μM amiloride. Furthermore, neither l- cis-diltiazem nor PsTx affected the β-adrenoceptor agonist-stimulated lung liquid absorption, but, as expected, amiloride completely ablated it. Thus, transport through alveolar CNGA1 channels, located in type I cells, underlies the amiloride-insensitive component of lung liquid reabsorption. Furthermore, our in situ data highlight the potential of CNGA1 as a novel therapeutic target for the treatment of diseases characterised by lung liquid overload. [ABSTRACT FROM AUTHOR]

ute myocardial infarction is a rare event in pregnant patients. Mechanical valves are naturally thrombogenic and require careful anticoagulation. Pregnancy produces a hypercoagulable situation and necessitates close follow-up in pregnant patients with mechanical heart valves. We present a 34-year-old pregnant woman who had mitral and aortic valve prosthesis. She developed resistant pulmonary oedema in the post-partum period after myocardial infarction. Oxytocin was used in this patient to induce midterm labour and prevent post-partum bleeding. Issues surrounding management of pulmonary oedema and use of oxytocin therapy during pregnancy are discussed. We emphasize the need for awareness of this condition and call attention to the risk of pulmonary oedema during labour. [ABSTRACT FROM AUTHOR]

Copyright of La Radiologia Medica is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Weaning-induced cardiogenic pulmonary oedema is a cause of weaning failure that is classically diagnosed by an increase in pulmonary artery occlusion pressure during a spontaneous breathing trial. During cardiogenic pulmonary oedema, a hypo-oncotic fluid is filtered toward the interstitial space. Thus, we tested whether the changes in plasma protein concentration during a weaning trial could diagnose weaning-induced pulmonary oedema. Prospective study. The 24-bed medical intensive care unit of a university hospital. Forty-six patients who had failed two weaning trials. Weaning-induced pulmonary oedema was diagnosed if a respiratory failure associated with an increase in pulmonary artery occlusion pressure above 18 mmHg occurred during a third weaning trial on a T-tube. The plasma protein concentration was measured before and at the end of the spontaneous breathing trial. During the weaning trial, pulmonary oedema was observed in 24 patients. In these patients, the plasma protein concentration increased by 11% (3–25%). The plasma protein concentration did not change significantly in patients who did not experience weaning-induced pulmonary oedema. An increase in the plasma protein concentration greater than 6% from baseline to the end of the weaning trial allowed detecting a weaning-induced pulmonary oedema with a sensitivity of 87% and a specificity of 95%. The acute changes in plasma protein concentration during a weaning trial represent an alternative method to right heart catheterisation for assessing weaning-induced pulmonary oedema. [ABSTRACT FROM AUTHOR]

Acute respiratory distress syndrome (ARDS) is characterized by sudden onset of respiratory distress, infiltrates on radiographs consistent with pulmonary oedema, hypoxaemia and increased work in breathing. Infiltrates on radiographs are bilateral, but may be patchy or diffuse and fluffy or dense. It is associated with absence of left heart failure and a PaO2/FiO2 ratio of ≤200. Ethylene vinyl alcohol copolymer dissolved in dimethyl sulfoxide (DMSO), which was approved by the US FDA in July 2005, is used as an embolic agent for cerebral arteriovenous malformation (AVM). It is a biocompatible liquid polymer that precipitates and solidifies on contact with blood, thus forming a soft and spongy embolus. We report a case of ARDS following therapeutic embolization with ethylene vinyl alcohol copolymer for cerebral AVM under general anaesthesia. Experienced perioperative physicians adopted standard anaesthetic technique and monitoring for this procedure. Acute respiratory distress and hypoxaemia developed in the patient following extubation of the trachea. Infiltrates seen on postprocedural chest radiographs were consistent with pulmonary oedema. DMSO, the solvent for the ethylene vinyl alcohol copolymer, is excreted via the lungs after administration and we postulate that DMSO was the possible cause of ARDS in this patient. Monitoring of haemodynamic parameters (invasive blood pressure, electrocardiography) and ventilatory parameters (ETCO2, SpO2, airway pressure monitoring) are important in the recognition of this possible event. One should be vigilant and anticipate this complication following therapeutic embolization with ethylene vinyl alcohol polymer for the treatment of cerebral AVM. [ABSTRACT FROM AUTHOR]

Copyright of Der Pneumologe is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Acute pulmonary oedema has been described in individuals participating in three aquatic activities: (i) scuba diving; (ii) breath-hold diving; and (iii) endurance swimming. In this review, 60 published cases have been compiled for comparison. Variables considered included: age; past medical history; activity; water depth, type (salt or fresh) and temperature; clinical presentation; investigations; management; and outcome. From these data, we conclude that a similar phenomenon is occurring among scuba, breath-hold divers and swimmers. The pathophysiology is likely a pulmonary overperfusion mechanism. High pulmonary capillary pressures lead to extravasation of fluid into the interstitium. This overperfusion is caused by the increase in ambient pressure, peripheral vasoconstriction from ambient cold, and increased pulmonary blood flow resulting from exercise. Affected individuals are typically healthy males and females. Older individuals may be at higher risk. The most common symptoms are cough and dyspnoea, with haemoptysis also a frequent occurrence. Chest pain has never been reported. Radiography is the investigation of choice, demonstrating typical findings for pulmonary oedema. Management is supportive, with oxygen the mainstay of treatment. Cases usually resolve within 24 hours. In some cases, diuretics have been used, but there are no data as to their efficacy. Nifedipine has been used to prevent recurrence, but there is only anecdotal evidence to support its use. [ABSTRACT FROM AUTHOR]

Measurement of lung water is an important diagnostic means of assessing pulmonary oedema. Water content affects the dielectric spectrum at microwave frequencies, but quantification is still a problem. A new lung tissue model is presented that allows the calculation of water content from dielectric permittivity. The dielectric permittivity of lung tissue was measured by microwave reflectometry using a non-invasive surface probe. During perfusion of rat lungs (n = 22) with blood, injury was induced by interruption of the blood supply for a duration between 0 (control) and 2 h. Water content was assessed from dielectric permittivity using a new mixture formula and was also determined by drying and weighing. The mixture formula allows for the dielectric polarisation of water, dry matter and air in the tissue. A linear correlation was found between total water content determined from dielectric permittivity and that from drying and weighing (y= 1.001x, R2 = 0.8). Lung injury showed an increase in total water content from 80.9 +/- 1.2% (control) to 84.1 +/- 0.9% (p < 0.01). The analysis of dielectric permittivity data at microwave frequencies with the new tissue model is sensitive enough to detect water accumulation produced by lung injury and it can be used to monitor total water content without tissue destruction. [ABSTRACT FROM AUTHOR]

Pulmonary oedema is a common sign of East Coast fever (ECF, Theileria parva infection) of cattle. A trial was conducted on farms in Uganda to compare a product containing both the antitheilerial compound parvaquone and the diuretic compound frusemide with one containing only parvaquone, in the treatment of ECF. The trial involved 40 clinical cases of ECF, some of them complicated by other infections, in cattle of all ages and on several farms. Confirmed cases were treated with either parvaquone + frusemide (P+F) or parvaquone alone (P). Survival after treatment with P+F was 77% compared with 71% with P. Five of the 10 fatalities were complicated cases. The cure rate for severe but uncomplicated ECF was 89% with P+F and 40% with P. Pulmonary signs were resolved within 24–48 h after treatment with P+F and clinical recovery was noticeably more rapid than with P. The antiparasitic effect of the two treatments was similar. P+F could be particularly useful when reporting, diagnosis or laboratory confirmation of ECF is delayed, because advanced cases are more likely to be encountered under these circumstances. [ABSTRACT FROM AUTHOR]

Objective: To explore the myocardial perfusion by thallium-201 scintigraphy for patients with evidence of myocardial damage after scorpion envenomation.Design: Prospective study over 1-year period.Setting: Medical intensive care unit of a university hospital (Sfax, Tunisia).Patients: We have prospectively included six patients admitted for scorpion envenomation over a period of 1 year in the 22-bed intensive care unit (ICU) of our university hospital. The evidence of myocardial damage was confirmed by electrocardiography and echocardiography in all patients. Myocardial perfusion scintigraphy ((201)Tl scintigraphy) coupled with radionuclide ventriculography ((99m)Tc) was performed for all patients, occurring 32 h on average (range 12-72 h) after the sting.Results: Radionuclide ventriculography was abnormal in all cases; the abnormalities observed were similar to those observed by echocardiography. Moreover (201)Tl scintigraphy showed evidence of myocardial hypoperfusion in all cases. The myocardial hypoperfusion grade and localisation were more marked in the abnormal localisation shown by echocardiography and electrocardiography, compared to the normal wall. Repeated studies, obtained only in two patients within 6 and 15 days, respectively, showed considerable, but not complete, improvement of wall motion and myocardial perfusion. Segments with improved perfusion showed greatly improved regional wall motion.Conclusion: This study confirms the evidence of myocardial hypoperfusion after severe scorpion envenomation. [ABSTRACT FROM AUTHOR]

Unlabelled: We studied the clinical and biochemical factors associated with surfactant dysfunction and factors affecting the responsiveness to exogenous surfactant among 27 neonates with haemorrhagic pulmonary oedema (HPE). HPE was defined as the presence of a large amount of blood-stained lung effluent and respiratory failure which was difficult to differentiate from respiratory distress syndrome. Among the neonates, 33% had very low birth weight, 96% were preterm, 70% were delivered by caesarean section, and 44% had delivery room intubation. The onset of HPE was at 1.5+/-0.1 h (mean +/- SEM) after birth. In 26 cases, surfactant was administered at 3.0+/-1.3 h after the onset of HPE. The concentrations of surfactant protein A (SP-A), disaturated phosphatidylcholine (DSPC), and albumin in the epithelial lining fluid were determined using the first lung effluent from the patients. The level of inhibitory activity against pulmonary surfactant in the effluent was determined in vitro. Surfactant inhibitory activity was associated with lower birth weight, earlier gestational age, delivery room intubation, earlier onset of HPE, and lower SP-A or DSPC concentration. A good response to exogenous surfactant, which was defined as ventilatory index <0.047 at 1 h after surfactant administration, was seen in 82% of cases, and was associated with lower serum albumin, lower birth weight, and earlier gestational age. Cases with higher DSPC concentration prior to surfactant administration and shorter interval between the onset of HPE and surfactant administration showed an immediate response to surfactant, followed by no increase in ventilatory index for 24 h after surfactant administration.Conclusion: exogenous surfactant appeared to be a useful adjunctive therapy for overcoming surfactant inhibition and normalising the respiratory status of infants with haemorraghic pulmonary oedema. Surfactant treatment for this indication awaits further investigations including a randomised controlled study. [ABSTRACT FROM AUTHOR]

Objective: To compare a molecular double-indicator dilution technique with the gravimetrical reference method for measurement of extra-vascular lung water in porcine endotoxin shock.Design: Open comparative experimental study.Setting: Animal research laboratory.Measurements and Results: In fourteen anaesthetised, mechanically ventilated landrace pigs, central and pulmonary haemodynamics as well as pulmonary gas exchange were measured. Extra-vascular lung water was quantitated gravimetrically as well as with a molecular double indicator dilution technique. Eight of these animals were subjected to endotoxaemia, the rest serving as sham controls. No difference in extra-vascular lung water was observed between the two methods in sham animals. Furthermore, extra-vascular lung water assessed with the molecular double-indicator dilution technique at the initiation of endotoxin infusion did not differ significantly from the corresponding values for sham animals. Endotoxaemia induced a hypodynamic shock with concurrent pulmonary hypertension and a pronounced deterioration in gas exchange. No increase in extra-vascular lung water was detected with the molecular double-indicator dilution technique in response to endotoxin, whereas this parameter was significantly higher when assessed with the gravimetric method.Conclusion: The molecular double-indicator dilution technique showed similar results as the gravimetrical method for assessment of extra-vascular lung water in non-endotoxaemic conditions. However, during endotoxin-induced lung injury the molecular double indicator dilution technique failed to detect the significant increase in extra-vascular lung water as measured by the gravimetric method. These data suggest that the molecular double indicator dilution technique may be of limited value during sepsis-induced lung injury. [ABSTRACT FROM AUTHOR]

Hydropericardium hepatitis syndrome in broiler chickens is an acute, infectious disease characterized by high mortality, excess pericardial fluid and multifocal hepatic necrosis. The aetiological agent was purified to homogeneity from infected liver tissues from field outbreaks. Electron-microscopic and serological confirmation of the virus were undertaken and the disease was reproduced experimentally in broiler chicks. The results indicated that an adenovirus, fowl adenovirus serotype 4, was alone responsible for the disease in the materials studied. [ABSTRACT FROM AUTHOR]

An intact alveolar epithelial barrier is thought to be important for alveolar liquid absorption. However, polycations increase alveolar permeability without affecting alveolar liquid absorption (Saumon et al., Am J Physiol 1995; 269:L185–L194). We have reconsidered this issue using polyamines. The polyamine spermine (10–3 mol/l) produced a large (up to 20-fold), sustained increase in the permeability of the alveolar barrier to mannitol (PAMan) and in alveolar liquid absorption (Jw, twofold) in isolated rat lungs. These increases were inhibited by 5·10–3 mol/l putrescine and 2·10–3 mol/l spermidine. Because spermine is known to affect the phosphoinositide/Ca2+ signalling pathway, we evaluated the effects of thiol reagents known to interfere with this pathway in different ways. Thimerosal, a thiol reagent which sensitizes the inositol 1,4,5-trisphosphate (IP3) receptor, inhibited the spermine-induced increase in PAMan and, to a lesser extent, that of Jw. Mersalyl, a thiol reagent which blocks IP3-gated Ca2+ channels, enhanced spermine's effect, whereas N-ethylmaleimide, a non-specific thiol reagent, had no effect. These observations show that large increases in permeability may coexist with increases in Jw. They also suggest that the phosphoinositide/Ca2+ second messenger pathway is involved in modulating the tightness of the alveolar barrier and alveolar liquid absorption. [ABSTRACT FROM AUTHOR]

Objectives: To investigate the relationship between the attenuation of impedance cardiac output (IC(co)) measurements and lung fluid content in critically ill patients.Design: Observational study.Setting: Intensive Care Unit of a major teaching hospital in Hong Kong.Patients: Twenty-four critically ill patients who required a pulmonary artery catheter.Measurements and Main Results: Triplicate thermodilution cardiac output (TD(co)) and BoMed NCCOM3 (IC(co)) measurements were made simultaneously on a single occasion in each patient. Lung fluid accumulation was assessed by: (a) thoracic impedance (Zo), (b) radiological assessment of chest X-rays using an alveolar consolidation score (0-4) and (c) scoring the degree of hypoxia and use of positive end-expiratory pressure (PEEP). Offsets (TD(co)-IC(co))/TD(co), expressed as percentage, were compared with these indices of excess lung fluid. Patients were divided into those with sepsis (n = 13), fluid balance problems (n = 5) and cardiothoracic problems (n = 6). Mean cardiac output values were: 6.7 l/min TD(co) (range 3.6-12.9) and 5.2 l/min IC(co) (range 2.7-9.0). Overall the TD(co) and IC(co) values showed great variance, with a bias and limits of agreement of 1.49 +/- 4.16 l/min, or +/- 69%. In septic patients, increasing offset was correlated with decreases in Zo (r = 0.73, P = 0.005) and increases in alveolar consolidation score (r = 0.72, P = 0.005).Conclusions: The BoMed under-estimates cardiac output in critically ill patients. In septic patients the degree of attenuation of IC(co) can be related to the extent of lung injury and fluid accumulation within the thorax. [ABSTRACT FROM AUTHOR]

Children permanently exposed to hypoxia at altitudes of >3000 m above sea level show a phenotypical form of adaptation. Under these environmental conditions, oxygen uptake in the lungs is enhanced by increases in ventilation, lung compliance, and pulmonary diffusion. Lung and thorax volumes in children growing up at high altitude are increased. The haemoglobin concentration in highlanders is evevated. With respect to the decreased arterial oxygen tension at high altitude, this seems a useful adaptation. Blood viscosity also increases as a result of the increase in red blood cell concentrations however, and this has potentially negative effects on the microcirculation in the tissues. The decreased partial pressure of oxygen in the lungs of highland children is associated with a higher pulmonary artery pressure. Pulmonary hypertension, high altitude pulmonary oedema, and chronic mountain sickness form part of the pathophysiology afflicting highland dwellers. Birth weight at high altitude is decreased. Decreased postnatal growth has been widely reported in populations at high altitude, particularly in early studies from the Andes. Recent studies taking into account the effects of socio-economic deprivation, suggest that long-term exposure to altitudes of 2500-3900 m is associated with a moderate reduction in linear growth in children. [ABSTRACT FROM AUTHOR]

In 35 present women, undergoing tocolytic treatment with betamimetics had intensive monitoring by balloon-tipped catheter. After the administration of 2-4 μg/min of fenoterol the cardiac output (CO) increased from 8.2 l/min to over 11 l/min with a corresponding increase in mean pulmonary artery pressure (MPAP) from 11.7 mmHg to over 18 mmHg. The correlation coefficient between MPAP/CO was highly significant. In the 10 patients in whom we were able to monitor pulmonary capillary pressure (PCP), we observed no significant increase to suggest compromised cardiac performance. The calculated total resistance of the pulmonary vessels (TPR) decreased during the first 24h followed by a return to initial values. Our investigations suggest that the principal cardiovascular effect of betamime-tics in pregnant women is a volume-dependent increase in pressure in the pulmonary circulation. The simultaneous administration of betamethasone had no additional effects. [ABSTRACT FROM AUTHOR]

Objective: To assess the accuracy of the diffusible indicators heavy water and thermal indicator in the measurement of extravascular lung water (EVLW).Design: Cardiac output (CO), mean transit time and EVLW for the two diffusible indicators were measured. CO for indocyanine green, gravimetric EVLW and the calculated mean transit time for a diffusible indicator were used as independent reference variables. CO, mean transit time and EVLW for the two diffusible indicators were compared to the reference variables and the percentage error for each measured variable was calculated for each bolus injection.Setting: 6 sheep with healthy lungs and 6 with pulmonary oedema in a research laboratory.Interventions: CO was altered with positive end-expiratory pressure and dobutamine.Measurements: All indicators were given together in a bolus through a central venous line. Indicators were detected simultaneously in the aorta, and CO, mean transit time and EVLW were measured. EVLW was measured gravimetrically (EVLWgrav) postmortem.Results: In the combination of a low CO and a large distribution volume, heavy water and thermal indicator produced a large number of slow wash-out curves. These curves were abolished from further analysis. The mean errors in CO and mean transit time for heavy water were close to zero and independent of the distribution volume; the product EVLW was close to EVLWgrav. The mean error in thermodilution CO measured in the aorta was close to zero but dependent on the distribution volume. The mean error in mean transit time for the thermal indicator was 36% and dependent on the distribution volume. Their product EVLW overestimated EVLWgrav by 70%.Conclusions: The results obtained for heavy water confirmed the theoretical basis of the indicator dilution method. The mean transit time for the thermal indicator was not proportionate to its distribution volume. The magnitude of this error prevents the calculation of an anatomically defined EVLW using a catheter-mounted thermistor in the aorta. [ABSTRACT FROM AUTHOR]

Objective: The identification of risk factors contributing to the development of pulmonary oedema, pneumonia and late mortality in submersion victims. Design: A retrospective study of 125 submersion victims. Setting: The medical intensive care unit in a university hospital. Methods: Baseline examination on admission consisted of history, physical examination, arterial blood gas analysis and a chest radiograph. Patients were then classified into four groups: class I, baseline examination negative; class II, baseline examination positive, but mechanical ventilation not needed on admission; class III, mechanical ventilation required on admission; class IV, patients suffering form cardiopulmonary arrest. All patients who were not succesfully resuscitated or who had expired with-in 24 h after admission were excluded for determination of the risk of pulmonary oedema and pneumonia. Results: Class I patients did not develop pulmonary complications; neither pulmonary oedema nor pneumonia occurred in this group. In the remaining classes the incidence of pulmonary oedema was 72% and that of pneumonia, 14.7%. Stepwise logistic regression showed that pulmonary oedema was related to the type of water (seawater, ditch water, swimming pool) victims were submerged in and to the neurological state both at the time of rescue and on admission. The development of pneumonia was related to the use of mechanical ventilation (the risk was 52%). Pneumonia was not related to neurological state at the time of rescue or on admission, to body temperature on admission, to the prohylactic administration of antibiotics or to the use of corticosteroids. Mortality was high in class IV patients, but low in all other patients. Early mortality was 18.4% while late mortality was 5.6%. Conclusions: There is no need to hospitalise submersion victims when there are no signs or symptoms of aspiration upon arrival in the emergency room. All other patients should be admitted to an intensive care unit. The risk of pneumonia is high when mechanical ventilation is necessary. Mortality is high in patients with circulatory arrest on admission, but low in all other patients. [ABSTRACT FROM AUTHOR]

A new model for selective sampling of thoracic lymph flow (TLF) and abdominal lymph flow (TDA) in the dog was assessed to ascertain whether there were extrathoracic contributions of lymph to the TLF. Inflating a right atrial balloon in 4 dogs and a left atrial balloon in 2 dogs indicated good separation between TLF and TDA. Data on total lymph protein and albumin clearance before and after oleic acid induced pulmonary oedema in an additional 5 dogs indicated that TLF and TDA drained two differing regions. Our data demonstrate that this lymph preparation provides a sample of thoracic lymph flow with no major extrathoracic lymph contamination. We also propose an alternative method to test for extrathoracic contributions to thoracic lymph, by the application of positive end-expiratory pressure, thereby replacing right atrial balloon inflation. [ABSTRACT FROM AUTHOR]

PEEP impedes thoracic duct drainage (LF). This can be counteracted by a thoracic duct fistula. Consequently, lung oedema (LOE) should develop during PEEP more slowly with LF at atmospheric pressure (LFAP) than with LF against jugular venous pressure (LFJVP). In 12 anaesthetized dogs LOE was produced by Ringer's solution i.v. (2.5 ml/min per kg) for 6 h during PEEP (10 mmHg) with either LFAP or LFJVP. Ringer's + PEEP greatly increased aortic, pulmonary artery and wedge pressures, JVP, and cardiac output. Colloid osmotic pressures in plasma and lymph were drastically reduced, pulmonary effective filtration pressure (EFP) rose by about 20 mmHg. LFJVP increased 7-fold, LFAP about 19-fold, the respective loss of plasma proteins was 1.83 and 1.06 g/kg during 6 h. Thermal-dye extravascular lung water showed an increment of 68 with LFJVP versus 43 microliter/h/g per mmHg with LFAP. Final lung water content was at any delta EFP (12.8-31.9 mmHg) lower with LFAP than with LFJVP amounting 512 with LFJVP versus 377 microliters/g/per mmHg with LFAP. LFAP decreased the development of LOE during PEEP by bypassing the PEEP-induced high JVP and thus facilitating the removal of interstitial fluid. It is hypothesized that a thoracic duct fistula might aid the treatment of patients with LOE due to ARDS and therefore requiring high levels of PEEP. [ABSTRACT FROM AUTHOR]

Plasma colloid osmotic pressure (COP) has been calculated from both serum albumin concentration and plasma total protein concentration. These values have been compared to those measured directly using a membrane-transducer oncometer in a group of normal subjects, in a group of critically-ill patients with a variety of primary diagnoses and in a group of hypovolaemic patients before and after plasma volume replacement with 6% hydroxyethyl starch solution. In the normal samples, COP calculated from albumin (COPalb) underestimated the measured COP (COPm) by mean of 2.0 mmHg (p less than 0.002), with correlation coefficient r = 0.39(n/s). Similarly, the COPalb underestimated COPm by a mean of 5.7 mmHg (p less than 0.001) in the critically ill patient group; r = 0.38 (p less than 0.02). Furthermore, in the patients receiving plasma volume replacement serum albumin concentration fell by 13.1% (p less than 0.001) whilst COPm increased by 11.5% (p less than 0.002). In the normal subjects COP calculated from total protein concentration (COPtp) underestimated the COPm by 1.5 mmHg (p less than 0.02) with r = 0.65 (p less than 0.01). Conversely, in the patient samples, mean COPtp overestimated COPm by 3.5 mmHg (p less than 0.001) with r = 0.73 (p less than 0.002). We conclude that COPalb is an inadequate estimate of COPm particularly in patients where its use may have important clinical consequences. COPtp provides a reasonable estimate of COPm in normal subjects but in patients samples, where albumin: globulin ratio is low COPtp overestimates substantially in many cases. We advocate the direct measurement of COP in critically-ill patients. [ABSTRACT FROM AUTHOR]

Acute mountain sickness is a condition affecting otherwise healthy individuals on going rapidly to altitude. It is caused by sub-acute hypoxia in susceptible subjects. Its study may provide lessons for the more complicated situation of hypoxia in patients undergoing intensive care. This paper reviews the incidence and aetiology of acute mountain sickness, pulmonary and cerebral oedema of high altitude and possible mechanisms are discussed. Prophylaxis depends on an awareness of the condition in all those venturing to high altitude and guidelines are suggested. The treatment of the established condition is reviewed. [ABSTRACT FROM AUTHOR]

Histological and physiological evidence suggests that in pulmonary ooedema the sequence of fluid accumulation in the lung is quantal (all-or-one). We have proposed that increased variation in radiographic density with respiration in pulmonary oedema can be attributed to quantal alveolar behaviour: the more severe the oedema, the greater the variation. To test this hypothesis CT scans of the chest were performed in 5 pigs on inspiratory and expiratory breath-holding at baseline and at various degrees of oleic acid pulmonary oedema. Extravascular lung water (EVLW) was monitored with the double indicator dilution technique to match these observations. At baseline, during induction and throughout the course of pulmonary oedema variation of radiographic attenuation with respiration correlated well with EVLW ( R = 0.98). With extensive alveolar oedema this variation did not match EVLW. It is concluded that the principle of quantal alveolar behaviour is a useful model for analysis of pulmonary oedema and its realtionship with respiration. [ABSTRACT FROM AUTHOR]

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Mast cell densities in the lung were measured in five native highlanders of La Paz (3600 m) and in one lowlander dying from high-altitude pulmonary oedema (HAPO) at 3440 m. Two of the highlanders were mestizos with normal pulmonary arteries and the others were Aymara Indians with muscular remodelling of their pulmonary vasculature. The aim of the investigation was to determine if accumulation of mast cells in the lung at high altitude (HA) is related to alveolar hypoxia alone, to a combination of hypoxia and muscularization of the pulmonary arterial tree, or to oedema of the lung. The lungs of four lowlanders were used as normoxic controls. The results showed that the mast cell density of the two Mestizos was in the normal range of lowlanders (0.6-8.8 cells/mm). In the Aymara Indians the mast cell counts were raised (25.6-26.0 cells/mm). In the lowlander dying from HAPO the mast cell count was greatly raised to 70.1 cells/mm lung tissue. The results show that in native highlanders an accumulation of mast cells in the lung is not related to hypoxia alone but to a combination of hypoxia and muscular remodelling of the pulmonary arteries. However, the most potent cause of increased mast cell density in the lung at high altitude appears to be high-altitude pulmonary oedema. [ABSTRACT FROM AUTHOR]

Chest-X-ray films of 61 children with isolated total anomalous pulmonary vein connection (TAPVC) were re-evaluated retrospectively. A small heart silhouette with normal pulmonary perfusion and signs of pulmonary oedema is typical of TAPVC with obstruction. There is no typical pattern in TAPVC without obstruction. The "snowman" or "figure of eight" does not develop within the first months of life. [ABSTRACT FROM AUTHOR]

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Copyright of Canadian Anaesthetists' Society Journal is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Pulmonary microemboli may play a role in the adult respiratory distress syndrome, creating both pulmonary oedema and hypoxaemia. We measured the time course of pulmonary oedema and hypoxaemia after pulmonary microemboli of 63-74 μ starch were infused into dogs. Dogs were divided into two groups: six dogs that did not develop pulmonary oedema, and seven that did. Immediately after emboli there was no difference between groups in the large fall in PaO or the rise in $$\dot Qs/\dot Qt$$ . Therefore the hypoxaemia of pulmonary embolism is not created by pulmonary oedema. As pulmonary oedema increased with time in the oedematous dogs, PaO fell further. There was no further reduction in PaO in the dogs who did not develop pulmonary oedema. We conclude that hypoxaemia after pulmonary embolism may be worsened if pulmonary oedema occurs, but the immediate large reduction in PaO after embolism is not created by pulmonary oedema. Les microembolies pulmonaires peuvent jouer un rôle important dans le syndrome d'insuffisance respiratoire des adultes en créant à la fois l'œdème pulmonaire et l'hypoxémie. Nous avons mesuré l'effet del'action de l'œdème pulmonaire et del'hypoxémie après que des chiens furent injectés avec des microembolies daamidon (63-73 μ), Les chiens éraient divisés en deux groupes: un des ces groupes était composé de sept chiens qui développèrent l'œdème pulmonaire et l'autre de six chiens qui ne le développèrent pas. Immédiatement après l'injection des embolies, on ne trouva pas de différence entre les deux groupes par rapport à la chute importante du PaO ou par rapport à la hausse du $$\dot Qs/\dot Qt$$ . Par conséquent, l'hypoxémie de l'embolisme pulmonaire ne résulte pas de l'œdème pulmonaire. A mesure que les ædèmes pulmonaires augmentèrent avec le temps chez les chiens cedémateux, le PaO chuta plus bas. Il nay eut plus de réduction dans le PaO chez les chiens qui naavaient pas développé daœdème pulmonaire. Nous concluons que l'hypoxémie après embolisme pulmonaire peut être empiréc sail y a œdème pulmonaire, mais la réduction immédiate du PaO après l'embolisme ne résulte pas de l'œdème pulmonaire. [ABSTRACT FROM AUTHOR]

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Copyright of Archiv für Toxikologie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

A 3-year-old male crossbreed dog presented with 1-week history of external otitis. During the initial clinical examination, the dog appeared alert and bright and there was no sign of other abnormalities. Ketamine was administered intramuscularly to induce a light sedation in order to perform otoscopic examination. Fifteen minutes following ketamine administration, the dog showed severe respiratory distress. Thoracic auscultation and radiography revealed the occurrence of pulmonary oedema secondary to adverse side effects of ketamine injection. Electrocardiographic findings showed low-voltage QRS complexes which continued, monitored via electrocardiograms, over the clinical course of the respiratory distress. This eletrocardiographic pattern disappeared completely the following day concurrent with the resolution of any respiratory distress. In view of the widespread use of ketamine by veterinary surgeons, the aim of this report is to contribute towards an increased awareness relating to unusual secondary cardiorespiratory effects of ketamine within the veterinary practice. [ABSTRACT FROM AUTHOR]

A young patient with a phaeochromocytoma who presented as an acute non cardiogenic pulmonary oedema is described. Phaeochromocytoma should be considered as a possible cause of the 'adult respiratory distress syndrome'. [ABSTRACT FROM AUTHOR]

A patient with gross pulmonary oedema secondary to inhalation of paint fumes is described. Treatment with mechanical ventilation and positive end expiratory pressure was required. [ABSTRACT FROM AUTHOR]

A sixteen month old girl developed acute respiratory failure from pulmonary oedema, and acute circulatory failure, following postoperative laryngeal obstruction. Her condition deteriorated despite mechanical ventilation with PEEP. She was finally treated with a combination of mild hypothermia, profound muscle paralysis and deep sedation for five days, after which she made a full recovery. This case confirms the previously reported value of such therapy when standard measures fail. [ABSTRACT FROM AUTHOR]

Background: Swimming-induced pulmonary oedema (SIPE) can affect people with no underlying health problems, but may be life threatening and is poorly understood. The aim of this systematic review was to synthesise the evidence on SIPE incidence, prevalence, risk factors, short- and long-term outcomes, recurrence and effectiveness of interventions to prevent recurrences.Methods: We carried out a literature search using bibliographic databases and reference lists. Risk of bias was assessed by adapting existing quality assessment tools including those developed by the National Heart Lung and Blood Institute.Results: Nine studies met the inclusion criteria. Quantitative synthesis was not possible because of study heterogeneity. Five studies, which differed from each other in case definition, swimming environment, population characteristics and denominators, reported an incidence of 0.01% of UK triathlons raced over 5 years in unspecified swimming environments (one study, not fully reported, of men and women of unspecified age); 0.5% of river races swum over 3 days in Sweden (one study, of men and women up to the age of 70); and 1.8-26.7% of time trials in the sea around Israel (three studies of male teenage military trainees). One study reported that 1.4% of triathletes in the USA had experienced SIPE. One study found that hypertension, female sex, fish oil use, long course distance and another lower initial lung volumes and flows were risk factors for SIPE. A third study reported that higher mean pulmonary artery pressures and pulmonary artery wedge pressures, and lower tidal volumes were associated with SIPE. Three studies suggested that SIPE symptoms usually resolve within 24 h, although a restrictive deficit in lung function persisted for a week in one small study. We found no studies that reported deaths from SIPE. The single small study of longer-term outcomes reported no difference between affected and unaffected swimmers. Two studies suggested that around 30% of people report recurrences of SIPE. Two very small uncontrolled studies of the effect of sildenafil for recurrence prevention were inconclusive.Conclusions: SIPE may be an important public health problem affecting the growing number of recreational open water swimmers. Further research should clarify the frequency of SIPE among recreational open water swimmers, confirm reported risk factors and explore others, explore long-term consequences and test interventions to prevent recurrences. [ABSTRACT FROM AUTHOR]

Venous air embolism (VAE) is a well known complication in procedures where the operative field is above the level of the heart. Acute pulmonary oedema after a large air embolus occurring during neurosurgery is also a recognized phenomenon. However, pulmonary oedema following repeated episodes of VAE in sublabial transsphenoidal (SLTS) surgery for pituitary adenoma has never been reported. We describe a case of VAE in a 65 year old male undergoing SLTS surgery for pituitary adenoma. Following this, the patient had pulmonary oedema which resolved on supportive treatment. Pulmonary oedema as a result of VAE may go unrecognised intraoperatively but can lead to a significant postoperative morbidity. Early suspicion and recognition of VAE and institution of aggressive treatment will help to avoid fatal consequences. [ABSTRACT FROM AUTHOR]

Presents a letter to the editor on the medical case of acute respiratory failure after re-expansion of pulmonary edema localized to a lobe.

A non-fatal case of carbon tetrachloride poisoning by inhalation is reported. The major features were acute renal failure, myocarditis and pulmonary oedema with effusion. Treatment included artificial ventilation and peritoneal dialysis. [ABSTRACT FROM AUTHOR]