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Pulmonary Edema [keywords]
- Effects of Neostigmine Reversal of Nondepolarizing Neuromuscular Blocking Agents on Postoperative Respiratory Outcomes: A Prospective Study. [JOURNAL ARTICLE]
- Anesthesiology 2014 Sep 15.
We tested the hypothesis that neostigmine reversal of neuromuscular blockade reduced the incidence of signs and symptoms of postoperative respiratory failure.We enrolled 3,000 patients in this prospective, observer-blinded, observational study. We documented the intraoperativeuse of neuromuscular blocking agents and neostigmine. At postanesthesia care unit admission, we measured train-of-four ratio and documented the ratio of peripheral oxygen saturation to fraction of inspired oxygen (S/F). The primary outcome was oxygenation at postanesthesia care unit admission (S/F). Secondary outcomes included the incidence of postoperative atelectasis and postoperative hospital length of stay. Post hoc, we defined high-dose neostigmine as more than 60 μg/kg and unwarranted use of neostigmine as neostigmine administration in the absence of appropriate neuromuscular transmission monitoring.Neostigmine reversal did not improve S/F at postanesthesia care unit admission (164 [95% CI, 162 to 164] vs. 164 [161 to 164]) and was associated with an increased incidence of atelectasis (8.8% vs. 4.5%; odds ratio, 1.67 [1.07 to 2.59]). High-dose neostigmine was associated with longer time to postanesthesia care unit discharge readiness (176 min [165 to 188] vs. 157 min [153 to 160]) and longer postoperative hospital length of stay (2.9 days [2.7 to 3.2] vs. 2.8 days [2.8 to 2.9]). Unwarranted use of neostigmine (n = 492) was an independent predictor of pulmonary edema (odds ratio, 1.91 [1.21 to 3.00]) and reintubation (odds ratio, 3.68 [1.10 to 12.4]).Neostigmine reversal did not affect oxygenation but was associated with increased atelectasis. High-dose neostigmine or unwarranted use of neostigmine may translate to increased postoperative respiratory morbidity.
- Risk assessment of ischemic stroke associated pneumonia. [Journal Article]
- World J Emerg Med 2014; 5(3):209-13.
Cerebral stroke is a disease with a high disability rate and a high fatality rate. This study was undertaken to assess the risk of stroke associated pneumonia (SAP) in patients with ischemic stroke using A2DS2 score.Altogether 1 279 patients with ischemic stroke who were treated in our department from 2009 to 2011 were retrospectively analyzed with A2DS2 score. A2DS2 score was calculated as follows: age ≥75 years=1, atrial fibrillation=1, dysphagia=2, male sex=1; stroke severity: NIHSS score 0-4=0, 5-15=3, ≥16=5. The patients were divided into three groups according to A2DS2 score: 620 in score 0 group, 383 in score 1-9 group, and 276 in score ≥10 group. The three groups were comparatively analyzed. The diagnostic criteria for SAP were as follows: newly emerging lesions or progressively infiltrating lesions on post-stroke chest images combined with more than two of the following clinical symptoms of infection: (1) fever ≥38 °C; (2) newly occurred cough, productive cough or exacerbation of preexisting respiratory tract symptoms with or without chest pain; (3) signs of pulmonary consolidation and/or wet rales; (4) peripheral white blood cell count ≥10×10(9)/L or ≤4×10(9)/L with or without nuclear shift to left, while excluding some diseases with clinical manifestations similar to pneumonia, such as tuberculosis, pulmonary tumors, non-infectious interstitial lung disease, pulmonary edema, pulmonary embolism and atelectasis. The incidence and mortality of SAP as well as the correlation with ischemic stroke site were analyzed in the three groups respectively. Mean± standard deviation was used to represent measurement data with normal distribution and Student's t test was used. The chi-square test was used to calculate the percentage for enumeration data.The incidence of SAP was significantly higher in the A2DS2 score≥10 group than that in the score 1-9 and score 0 groups (71.7% vs. 22.7%, 71.7% vs. 3.7%, respectively), whereas the mortality in the score≥10 group was significantly higher than that in the score 1-9 and score 0 groups (16.7% vs. 4.96%, 16.7% vs. 0.3%, respectively). The incidences of cerebral infarction in posterior circulation and cross-MCA, ACA distribution areas were significantly higher than those in the SAP group and in the non-SAP group (35.1% vs.10.1%, 11.4% vs. 7.5%, respectively). The incidence of non-fermentative bacteria infection was significantly increased in the score≥10 group.A2DS2 score provides a basis for risk stratification of SAP. The prevention of SAP needs to be strengthened in acute ischemic stroke patients with a A2DS2 score≥10.
- Differential diagnosis of a fulminant myocarditis: the pheochromocytoma crisis. [JOURNAL ARTICLE]
- Eur Heart J Acute Cardiovasc Care 2014 Sep 15.
Concurring left ventricular dysfunction, pulmonary edema and febrile temperature in otherwise healthy young individuals often constitutes the clinical presentation of a fulminant myocarditis. Nevertheless, the pheochromocytoma crisis (PCC) can mimic this very cluster of symptoms, camouflaging its disclosure. We describe a dramatic case of pheochromocytoma crisis mimicking fulminant myocarditis.
- Impact of patient positioning on lung ultrasound findings in acute heart failure. [JOURNAL ARTICLE]
- Eur Heart J Acute Cardiovasc Care 2014 Sep 15.
The purpose of this study was to compare lung ultrasound findings in both the supine and upright positions in heart failure patients presenting with dyspnea or chest pain.We performed lung ultrasonography on 50 heart failure patients in the emergency department. Each subject underwent eight-zone lung sonography in the seated upright position, followed by a repeat ultrasound in the supine position. Each ultrasound video clip was later assigned a score (0-2 B-lines=0 points, 3-7 B-lines=1 point, >7 B-lines=2 points) by a physician who was blinded to patient position, chest zone, and clinical information. The median B-line score on eight-zone lung ultrasound was significantly higher in the supine (6, interquartile range (IQR) 2-10) vs the sitting position (5, IQR 1-8; p<0.001). Subjects with vascular congestion or pulmonary edema on chest x-ray (CXR) (n=29) also had higher median eight-zone B-line scores in the supine position (6, IQR 4-10) compared to the sitting position (5, IQR 2-8; p=0.002). Subjects without any acute pulmonary findings on CXR (n=19) had similar median eight-zone B-line scores in sitting (4, IQR 1-7) and supine positions (4, IQR 1-9, p=0.093).Our findings suggest that patient positioning may impact the number of B-lines on lung ultrasound in a heart failure population. A consistent approach to patient positioning during lung ultrasonography may be necessary in order to monitor dynamic changes in heart failure.
- [Protective effect of an angiotensin-converting-enzyme inhibitor on neurogenic pulmonary edema in rabbits]. [English Abstract, Journal Article]
- Zhonghua Er Ke Za Zhi 2014 Aug; 52(8):602-6.
Neurogenic pulmonary edema (NPE ) was indicative of poor prognosis in the epidemic of enterovirus 71 infections. The pathogenesis of NPE remains poorly understood. The objectives of this experimental study were to explore whether RAS is activated during NPE in rabbit models induced by fibrin and the effects of an angiotensin converting enzyme inhibitor (enalaprilat) on NPE.NPE models were induced by intracisternal injection of fibrinogen and thrombin. According to random number table method, 18 healthy adult New Zealand rabbits were assigned to three groups (with 6 in each) : normal control group (Con group), NPE group and enalaprilat treated (Ena) group. After establishment of NPE models, rabbits in Ena group were given intravenous enalaprilat 0.5 mg/kg. Expression of ACE,ACE2,AT1R mRNA of the lung tissue were evaluated by real-time polymerise chain reaction; and Ang II of the lung tissue was determined by enzyme linked immunosorbent assay ( ELISA ). Meanwhile, histopathological lung injury scores were evaluated.ACE mRNA expression level in NPE group ( 17.2 ± 3.3) appeared an increasing trend in contrast to Con group ( 12.6 ± 5.2 ) and Ena group ( 11.5 ± 2.4, both P > 0.05 ). Compared with Con group (81 ± 22 ), ACE2 mRNA expression levels of NPE group ( 52 ± 6 ) and Ena group ( 45 ± 13 ) both decreased ( both P < 0.05 ) . ACE mRNA/ACE2 mRNA expression levels of NPE group ( 0.33 ± 0.06 ) and Ena group ( 0.26 ± 0.04 ) were higher than those of Con group ( 0.16 ± 0.05, both P < 0.05 ), as well as the ratio of Ena group decreased compared with untreated NPE group ( 0.26 ± 0.04 vs. 0.33 ± 0.06, P < 0.05 ) . There were no statistically significant differences in expression of AT1 mRNA of the lung tissue among three groups, but Ena group ( 4.8 ± 1.1) in contrast to NPE group ( 6.7 ± 1.3) has no significant difference (P > 0.05). Lung AngII level of NPE group [(540 ± 147) pg/ml] was significantly higher than that of Con group [(253 ± 37 ) pg/ml] and Ena group [(309 ± 35 ) pg/ml, both P < 0.05 ]. Gross pathologic examination showed that pink foamy edema fluid appeared in the tracheal tubes in NPE group, but spontaneously appeared in neither Con group nor Ena group; and the level of pulmonary subpleural bleeding in Con group, 12 graded 0; in NPE group, 2 graded II, 10 graded III; in Ena group, 2 graded, 8 grade II, 2 grade III. The histopathologic lung injury scores in Ena group was decreased in contrast to NPE group (1.36 ± 0.26 vs.2.32 ± 0.49, P < 0.05) and mainly for the improvement of alveolar overdistension and interstitial edema.The present study showed that when NPE occurs, a high lung AngII concentration was associated with an imbalance between ACE mRNA to ACE2 mRNA expression level. Activated local RAS in lung tissue resulted in lung injury. Enalaprilat treatment may attenuate lung injury by interventing local RAS in lung tissue with decreased ratio of ACE mRNA to ACE2 mRNA and lung AngII concentration. The result will be significant for the angiotensin converting enzyme inhibitor used in the theatment of NPE.
- [Negative pressure pulmonary edema with upper airway obstruction: analysis of 3 patients]. [English Abstract, Journal Article]
- Zhonghua Er Ke Za Zhi 2014 Jul; 52(7):531-4.
To investigate the clinical characteristics and treatment of negative pressure pulmonary edema (NPPE) with upper airway obstruction (UAO) in children.Data of 3 cases with NPPE and UAO in pediatric intensive care unit (PICU) from Mar, 2007 to May, 2013 were analyzed.(1) Two cases were male and 1 was female with age respectively 6, 16 and 30 months.One had airway foreign body , 1 laryngitis , and 1 retropharyngeal abscess. The onset of NPPE varied from 5 to 40 minutes following relief of obstruction. (2) NPPE presented with acute respiratory distress with signs of tachypnea, tachycardia, 2 of the 3 with pink frothy pulmonary secretions, progressively decreased oxygen saturation, rales on chest auscultation and wheezing. (3) NPPE chest radiograph showed diffuse interstitial and alveolar infiltrates, images confirmed pulmonary edema. (4) All these patients received these therapeutic measures including mechanical ventilation, retaining high PEEP, diuretics, limiting the fluid input volume to 80-90 ml/ (kg×d) on the basis of circulation stability. The rales on chest auscultation disappeared after 10, 6, 12 hours. The ventilators of 2 patients were removed within 24 hours, in another case it was removed 50 hours later because of secondary infection. All patients were cured and discharged without complication.NPPE progresses very fast, characterized by rapid onset of symptoms of respiratory distress after UAO, with pulmonary edema on chest radiograph. The symptoms resolve rapidly if early support of breath and diuretics are applied properly.
- Pulmonary venous hypertension and mechanical strain stimulate monocyte chemoattractant protein-1 release and structural remodelling of the lung in human and rodent chronic heart failure models. [JOURNAL ARTICLE]
- Thorax 2014 Sep 15.
The burden of chronic heart failure (HF) is rising owing to an increased survivorship after myocardial infarction (MI). Pulmonary structural remodelling in patients with HF may protect against oedema while causing dyspnoea, the predominant symptom associated with HF. The cellular and molecular mechanisms underlying these processes in HF are poorly understood. We hypothesised that pulmonary venous hypertension (PVH) following MI provides a mechanical stimulus for structural remodelling of the lung via monocyte chemoattractant protein-1 (MCP-1).Human lung microvascular endothelial cells (HLMVEC) and Ea.Hy 926 cells exposed to cyclic mechanical strain (CMS) in vitro were analysed for MCP-1 expression and activation of signalling intermediates. HF was induced in Sprague-Dawley rats 16 weeks after MI; a cohort was rescued with AAV9.SERCA2a gene therapy to reduce PVH.HLMVEC and Ea.Hy 926 cells exposed to CMS upregulated MCP-1 gene expression and protein release in an extracellular-signal-regulated kinase (ERK) 1/2 dependent manner. Supernatants from these experiments stimulated fibroblast (human fetal lung fibroblast -1) and pulmonary artery smooth muscle cell proliferation and differentiation. Total lung collagen, a marker of structural remodelling, and MCP-1 gene expression were increased in the lungs of rats with post-MI HF. SERCA2a gene therapy that attenuated PVH after MI was associated with lower levels of lung collagen and MCP-1 gene expression in the lung.Mechanical strain associated with PVH may stimulate pulmonary structural remodelling through ERK 1/2 dependent induction of MCP-1. These findings provide insights into the pathophysiology of lung remodelling in HF and highlight novel, potential therapeutic targets.
- Immersion Pulmonary Edema and Comorbidities: Case Series and Updated Review. [JOURNAL ARTICLE]
- Med Sci Sports Exerc 2014 Sep 12.
Immersion pulmonary edema occurs in swimmers (especially triathletes) and scuba divers. Its pathophysiology and risk factors are incompletely understood. This study was designed to establish the prevalence of pre-existing comorbidities in individuals who experience immersion pulmonary edema.From 2008 to May 2010, individuals who had experienced immersion pulmonary edema were identified via recruitment for a physiological study. Past medical history and subject characteristics were compared with those available in the current body of literature.At Duke University Medical Center, Durham, NC, 36 subjects were identified (mean age 48.4 ± 9.1 years), of whom 72.2% had one or more significant medical conditions at the time of IPE incident (e.g., hypertension, cardiac dysrhythmias or structural abnormality or dysfunction, asthma, diabetes mellitus, overweight or obesity, obstructive sleep apnea, hypothyroidism). Forty-five articles were included, containing 292 cases of IPE, of which 24.0% had identifiable cardiopulmonary risk factors. Within the recreational population, cases with identifiable risk factors comprised 44.9%. Mean age was 47.8 ± 11.3 in recreational divers/swimmers and 23.3 ± 6.4 years in military divers/swimmers.Cardiopulmonary disease may be a common predisposing factor in immersion pulmonary edema in the recreational swimming/diving population, while pulmonary hypertension due to extreme exertion may be more important in military cases. Individuals with past history of immersion pulmonary edema in our case series had a greater proportion of comorbidities compared to published cases. The role of underlying cardiopulmonary dysfunction may be underestimated, especially in older swimmers and divers. We conclude that an episode of immersion pulmonary edema should prompt evaluation of cardiac and pulmonary function.
- The Poly(Adenosine Diphosphate-Ribose) Polymerase Inhibitor PJ34 Reduces Pulmonary Ischemia-Reperfusion Injury in Rats. [JOURNAL ARTICLE]
- Transplantation 2014 Sep 27; 98(6):618-624.
Ischemia-reperfusion (I/R) injury after lung transplantation causes alveolar damage, lung edema, and acute rejection. Poly(adenosine diphosphate-ribose) polymerase (PARP) is a single-stranded DNA repair enzyme that induces apoptosis and necrosis after DNA damage caused by reactive oxygen species. We evaluated tissue protective effects of the PARP inhibitor (PARP-i) PJ34 against pulmonary I/R injury.Rats (total n=45) underwent a thoracotomy with left hilar isolation and saline administration (sham group) or thoracotomy with hilar clamping and saline administration (I/R group) or PJ34 administration (PARP-i group). Parameters were measured for 7 days after reperfusion.Pathologic analysis revealed that reperfusion injury was drastically suppressed in the PARP-i group 2 days after reperfusion. Terminal deoxynucleotide transferase-mediated deoxyuridine triphosphate nick-end labeling-positive cells were significantly decreased in the PARP-i group compared to the I/R group (P<0.05). Accordingly, the wet-to-dry lung ratio in the I/R group was significantly higher compared with the PARP-i group (P=0.025). Four hours after reperfusion, serum tissue necrosis factor-α and interleukin-6 were significantly suppressed in the PARP-i group compared with the I/R group (P<0.05). Serum derivatives of reactive oxygen metabolites increased quickly and remained high in the I/R and PARP-i groups from 4 hr until 7 days after reperfusion. Interestingly, the serum biologic antioxidant potential in the PARP-i group was significantly higher than that in the I/R group from day 2 until day 7.The PARP-i decreased inflammation and tissue damage caused by pulmonary I/R injury. These beneficial effects of the PARP-i may be correlated with its antioxidative efficacy.
- Paradoxical Use of Tumor Necrosis Factor in Treating Pulmonary Edema. [JOURNAL ARTICLE]
- Am J Respir Crit Care Med 2014 Sep 15; 190(6):595-596.