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Pulmonary Edema [keywords]
- Pathophysiology, clinical features and radiological findings of differentiation syndrome/all-trans-retinoic acid syndrome. [Journal Article, Review]
- World J Radiol 2014 Aug 28; 6(8):583-8.
In acute promyelocytic leukemia, differentiation therapy based on all-trans-retinoic acid can be complicated by the development of a differentiation syndrome (DS). DS is a life-threatening complication, characterized by respiratory distress, unexplained fever, weight gain, interstitial lung infiltrates, pleural or pericardial effusions, hypotension and acute renal failure. The diagnosis of DS is made on clinical grounds and has proven to be difficult, because none of the symptoms is pathognomonic for the syndrome without any definitive diagnostic criteria. As DS can have subtle signs and symptoms at presentation but progress rapidly, end-stage DS clinical picture resembles the acute respiratory distress syndrome with extremely poor prognosis; so it is of absolute importance to be conscious of these complications and initiate therapy as soon as it was suspected. The radiologic appearance resembles the typical features of cardiogenic pulmonary edema. Diagnosis of DS remains a great skill for radiologists and haematologist but it is of an utmost importance the cooperation in suspect DS, detect the early signs of DS, examine the patients' behaviour and rapidly detect the complications.
- Radiographically Severe but Clinically Mild Reexpansion Pulmonary Edema following Decompression of a Spontaneous Pneumothorax. [Journal Article]
- Case Rep Pulmonol 2014.:709560.
The case is a 48-year-old female who presented with mild dyspnea on exertion and cough with unremarkable vital signs and was found to have a large right sided pneumothorax. She underwent small bore chest tube decompression with immediate reexpansion of the collapsed lung. However, she rapidly developed moderate hypoxemia and radiographic evidence of reexpansion pulmonary edema (REPE) on both the treated and contralateral sides. Within a week, she had a normal chest X-ray and was asymptomatic. This case describes a rare complication of spontaneous pneumothorax and highlights the lack of correlation between symptoms, sequelae, and radiographic severity of pneumothorax and reexpansion pulmonary edema. Proposed pathophysiologic mechanisms include increased production of reactive oxygen species with subsequent loss of surfactant and increased vascular permeability, and loss of vasoregulatory tone.
- Successful venous angioplasty of superior vena cava syndrome after heart transplantation. [Journal Article]
- Case Rep Cardiol 2014.:490276.
Introduction.For patients with terminal heart failure, heart transplantation (HTX) has become an established therapy. Before transplantation there are many repeated measurements with a pulmonary artery catheter (PAC) via the superior vena cava (SVC) necessary. After transplantation, endomyocardial biopsy (EMB) is recommended for routine surveillance of heart transplant rejection again through the SVC. Case Presentation. In this report, we present a HTX patient who developed a SVC syndrome as a possible complication of all these procedures via the SVC. This 35-year-old Caucasian male could be successfully treated by balloon dilatation/angioplasty.
Conclusion.The SVC syndrome can lead to pressure increase in the venous system such as edema in the head and the upper part of the body and further serious complications like cerebral bleeding and ischemia, or respiratory problems. Balloon angioplasty and stent implantation are valid methods to treat stenoses of the SVC successfully.
- Acute lung injury after platelet transfusion in a patient with dengue fever. [Journal Article]
- Asian J Transfus Sci 2014 Jul; 8(2):131-4.
Transfusion-related acute lung injury (TRALI) is a serious clinical syndrome associated with the transfusion of plasmacontaining blood components. Recently, TRALI has come to be recognized as the leading cause of transfusion-related mortality. This complication typically presents as shortness of breath, hypoxemia, hypotension, fever, and non cardiogenic pulmonary edema, occurring within 6 h after transfusion. Although the mechanism of TRALI has not been exactly known, it has been associated with human leukocyte antigen antibodies and with biologically active mediators in stored cellular blood components. We, hereby, present a case of a patient with dengue fever who developed acute lung injury (ALI), presumably TRALI, after transfusion of platelet concentrates. He was treated with supportive measures and mechanical ventilation. Greater knowledge and increased awareness especially amongst the clinicians regarding TRALI is needed for prevention and treatment of this potentially severe complication of blood/component transfusion.
- Neurogenic pulmonary edema in pediatric multiple sclerosis: patient report and summary of cases. [Journal Article]
- Pediatr Neurol 2014 Sep; 51(3):426-9.
Neurogenic pulmonary edema may be a complication of multiple neurological processes. Although there is debate regarding the underlying pathophysiology, the recognition of neurogenic pulmonary edema is vitally important because of the high-potential for mortality and need for treatment of the underlying disorder.We present an example of recurrent neurogenic pulmonary edema in an adolescent boy with multiple sclerosis who was diagnosed with pneumonia at the time of initial presentation. We also review the presenting symptoms, physiologic parameters, and imaging findings from published reports of patients with multiple sclerosis presenting with neurogenic pulmonary edema.Although all 11 cases found via literature review presented with respiratory symptoms, cardiac dysfunction was variable, as was the presence of other neurological findings. All but one case had a documented medullary lesion. Corticosteroids were effective in resolving symptoms. Three patients were not treated with corticosteroids, and one of these died (onset of pulmonary edema during sleep).Awareness of these patients may expedite recognition and treatment of future patients, thus minimizing time to appropriate treatment and reducing mortality.
- Weaning the cardiac patient from mechanical ventilation. [JOURNAL ARTICLE]
- Curr Opin Crit Care 2014 Aug 23.
Because of heart-lung interactions, weaning from mechanical ventilation induces strong hemodynamic changes that can lead to weaning-induced cardiac failure. Cardiac patients are particularly at risk for this complication. In this review, we will summarize the most recent advances concerning the mechanisms, diagnosis and treatment of weaning-induced cardiac failure.The role of left ventricular diastolic abnormalities contributing to weaning-induced pulmonary edema has been recently emphasized. The most important recent findings concern the diagnostic tools that can be used as alternatives to the pulmonary artery catheter for detecting weaning-induced pulmonary edema during a spontaneous breathing trial, such as increase in estimates of left ventricular filling pressure with echocardiography, increase in B-type natriuretic peptide, increase in plasma protein and hemoglobin concentration and increase in extravascular lung water measured by transpulmonary thermodilution. Concerning the treatment, recent data suggest that fluid removal, which is often indicated in such instances, could be guided by the dosage of B-type natriuretic peptide.Nowadays, the diagnosis of weaning-induced pulmonary edema can be easily made. Identifying such an event is important as an appropriate treatment, guided by the suspected mechanisms leading to the cardiac failure, should hasten weaning from mechanical ventilation.
- Adenosine, lidocaine and Mg2+ (ALM) induces a reversible hypotensive state, reduces lung edema and prevents coagulopathy in the rat model of polymicrobial sepsis. [JOURNAL ARTICLE]
- J Trauma Acute Care Surg 2014 Sep; 77(3):471-478.
No drug therapy has demonstrated improved clinical outcomes in the treatment of sepsis. A bolus of adenosine, lidocaine, and magnesium (ALM) has been shown to be cardioprotective and restore coagulopathy in different trauma states. We hypothesized that ALM therapy may improve hemodynamics, protect the lung, and prevent coagulopathy in the rat sepsis model.Nonheparinized, anesthetized Sprague-Dawley rats (350-450 g, n = 32) were randomly assigned to (1) shams (without sepsis), (2) saline controls, and (3) ALM treatment. Sepsis was induced by cecal ligation and puncture. A 0.3-mL bolus was administered intravenously, followed by a 4-hour intravenous infusion (1 mL/kg/h), and hemodynamics (mean arterial pressure [MAP], systolic arterial pressure, diastolic arterial pressure, and heart rate [HR]) and body temperature (BT) were monitored. Coagulation was assessed using prothrombin time and activated partial thromboplastin time (aPTT).Shams displayed progressive falls in MAP, HR, and BT as well as a prolonged aPTT, which were related to surgery, not infection. At 4 hours, controls showed more pronounced falls in MAP (33%), HR (17%), and BT (3.3°C), and MAP continued to fall after the infusion was stopped. In contrast, ALM treatment resulted in a rapid fall in MAP from 111 mm Hg to 73 mm Hg at 30 minutes (p < 0.05 all groups) and was 59 mm Hg at 240 minutes (p < 0.05 shams), which immediately corrected after 4 hours (p < 0.05 controls). HR paralleled MAP changes in ALM rats, and BT was significantly higher than that of the controls but not that of shams. ALM rats had no arrhythmias compared with the controls or shams and had significantly lower lung wet-dry ratios. Prothrombin time in saline controls at 1 hour and 5 hours was prolonged but not in the shams or ALM rats. aPTT at 1 hour in the sham, control, and ALM groups was 158 ± 41 seconds, 161 ± 41 seconds, and 54 ± 23 seconds and at 5 hours was 104 ± 43 seconds, 205 ± 40 seconds, and 33 ± 3 seconds (p < 0.05), respectively.An ALM bolus/infusion induces a stable, hypotensive hemodynamic state with no arrhythmias, significantly less pulmonary edema, and a higher BT and prevents coagulopathy compared with the controls.
- [Update on current care guidelines: acute respiratory failure]. [English Abstract, Journal Article]
- Duodecim 2014; 130(14):1460-2.
Acute respiratory failure is the most common organ failure leading to need of intensive care. The incidence of acute respiratory failure in adult population is 78-89/100000/year and mortality is 35-40 %. The preferred treatment modality in acute respiratory failure related to exacerbation of COPD is noninvasive ventilation. NIV reduces mortality of COPD and pulmonary oedema patients compared to plain oxygen therapy. However, the evidence of NIV's effect on mortality in more heterogenous group of hypoxemic patients is scarce. Key recommendations conserning invasive ventilation is to avoid tidal volumes over 7 ml/bodyweight and to use at least 5 cm H2O of PEEP.
- New insights into the organ-specific adverse effects of fumonisin B1: comparison between lung and liver. [JOURNAL ARTICLE]
- Arch Toxicol 2014 Aug 26.
Fumonisin B1 (FB1) is a well-known inhibitor of de novo sphingolipid biosynthesis, due to its ability to inhibit ceramide synthases (CerS) activity. In mammals, this toxin triggers broad clinical symptoms with multi-organ dysfunction such as hepatotoxicity or pulmonary edema. The molecular mechanism of CerS inhibition by FB1 remains unknown. Due to the existence of six mammalian CerS isoforms with a tissue-specific expression pattern, we postulated that the organ-specific adverse effects of FB1 might be due to different CerS isoforms. The sphingolipid contents of lung and liver were compared in normal and FB1-exposed piglets (gavage with 1.5 mg FB1/kg body weight daily for 9 days). The effect of the toxin on each CerS was deduced from the analysis of its effects on individual ceramide (Cer) and sphingomyelin (SM) species. As expected, the total Cer content decreased by half in the lungs of FB1-exposed piglets, while in contrast, total Cer increased 3.5-fold in the livers of FB1-exposed animals. Our data also indicated that FB1 is more prone to bind to CerS4 and CerS2 to deplete lung and to enrich liver in d18:1/C20:0 and d18:1/C22:0 ceramides. It also interact with CerS1 to enrich liver in d18:1/C18:0 ceramides. Cer levels were counterbalanced by those of SM. In conclusion, these results demonstrate that the specificity of the effects of FB1 on tissues and organs is due to the effects of the toxin on CerS4, CerS2, and CerS1.
- Mortality in cardiogenic shock complicating acute myocardial infarction due to left main coronary artery disease: does gender matter? [Journal Article]
- Przegl Lek 2014; 71(3):117-21.
To assess prognosis in men and women with myocardial infarction (MI) complicated with cardiogenic shock (CS) due to critical stenosis of the unprotected left main coronary artery (ULMCA).A total of 643 (females 28.6%, males 71.4%) consecutive patients with critical ULMCA stenosis and acute MI were included. Data were obtained from the Polish Registry of Acute Coronary Syndromes (PL-ACS). Study end-points were defined as in-hospital death, mortality at 30 days, 6 and 12 months. Of all patients 103 (16.0%) developed CS. Basic characteristics and treatment strategy were similar in both sexes. As many as 95% of patients in CS were treated invasively with PCI. In-hospital mortality among women in CS was lower than among men (43.3% vs. 64.4%, p = 0.049). Mortality at 30 days and 12 months in CS group as well as in patients without CS did not differ significantly between men and women. In multivariate analysis age and CS, but not a female gender, were independent factors of increased mortality whereas only a successful PCI significantly reduced mortality.Cardiogenic shock and pulmonary edema were independent factors of mortality. There were no differences in mortality between men and women in subgroups with and without CS. Emergency PCI seems to be a useful and beneficial option in this subset of patients.