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Pulmonary Edema [keywords]
- [Transfusion-related Acute Lung Injury (TRALI).] [JOURNAL ARTICLE]
- Pneumologie 2014 Jul 21.
Transfusion-related acute lung injury (TRALI) is primarily caused by transfusion of fresh frozen plasma or platelet concentrates and occurs by definition within 6 hours after transfusion with acute shortness of breath, hypoxemia and radiographically detectable bilateral infiltrates of the lung. Mostly leucocyte antibodies in the plasma of the blood donor (immunogenic TRALI) are responsible. Apart from antibodies, other substances such as biologically active lipids, mainly arising from the storage of platelet and red blood cell concentrates, can activate neutrophilic granulocytes and trigger a non-immunogenic TRALI. Pathophysiologically, granulocytes in the capillaries of the lung vessels release oxygen radicals and enzymes which damage the endothelial cells and cause pulmonary edema. Therapeutically, nasal oxygen administration may be sufficient. In severe cases, mechanical ventilation, invasive hemodynamic monitoring and fluid intake are required. Diuretics should be avoided. The administration of glucocorticoids is controversial. Antibody-related TRALI reactions occurred mainly after transfusion of fresh frozen plasma, which had been obtained from womenimmunized during pregnancy against leukocyte antigens. Therefore, in Germany, since 2009 only plasma from female donors without a history of prior or current pregnancy or negative testing for antibodies against HLA I, II or HNA has been used with the result that since then no TRALI-related death has been registered.
- An integrated physiology model to study regional lung damage effects and the physiologic response. [JOURNAL ARTICLE]
- Theor Biol Med Model 2014 Jul 21; 11(1):32.
This work expands upon a previously developed exercise dynamic physiology model (DPM) with the addition of an anatomic pulmonary system in order to quantify the impact of lung damage on oxygen transport and physical performance decrement.A pulmonary model is derived with an anatomic structure based on morphometric measurements, accounting for heterogeneous ventilation and perfusion observed experimentally. The model is incorporated into an existing exercise physiology model; the combined system is validated using human exercise data. Pulmonary damage from blast, blunt trauma, and chemical injury is quantified in the model based on lung fluid infiltration (edema) which reduces oxygen delivery to the blood. The pulmonary damage component is derived and calibrated based on published animal experiments; scaling laws are used to predict the human response to lung injury in terms of physical performance decrement.The augmented dynamic physiology model (DPM) accurately predicted the human response to hypoxia, altitude, and exercise observed experimentally. The pulmonary damage parameters (shunt and diffusing capacity reduction) were fit to experimental animal data obtained in blast, blunt trauma, and chemical damage studies which link lung damage to lung weight change; the model is able to predict the reduced oxygen delivery in damage conditions. The model accurately estimates physical performance reduction with pulmonary damage.We have developed a physiologically-based mathematical model to predict performance decrement endpoints in the presence of thoracic damage; simulations can be extended to estimate human performance and escape in extreme situations.
- Prenatal management and outcomes in mirror syndrome associated with twin-twin transfusion syndrome. [JOURNAL ARTICLE]
- Prenat Diagn 2014 Jul 9.
To investigate the prevalence, clinical presentation, prenatal management and prognosis of mirror syndrome associated with twin-twin transfusion syndrome (TTTS) treated by amnioreduction or selective fetocide.A retrospective study of twin pregnancies with TTTS was conducted. The prevalence of mirror syndrome, defined as severe maternal edema related to fetal hydrops and placental edema, was calculated for TTTS, and data on clinical characteristics, treatment and outcomes of the patients were reviewed.We observed mirror syndrome in 4.85% (5/103) of pregnancies with TTTS and 26.32% (5/19) of pregnancies with TTTS Stage IV. Most cases (4/5) of mirror syndrome associated with TTTS were diagnosed before 24 weeks of gestation. The patients manifested edema, anemia, hemodilution and hypoproteinemia (5/5), proteinuria (4/5), complicated postpartum hemorrhage (4/5), pulmonary edema and congestive heart failure (2/5). Maternal hemoglobin, hematocrit and plasma protein dropped after amnioreduction. The perinatal survival rate at 28 days was 28.57% (2/7), and only 1 infant born after selective feticide survived beyond 18 months.TTTS carries a high risk of mirror syndrome, a disease with significant materno-fetal mortality and morbidity. Amnioreduction alone or with selective feticide in mirror syndromemay transiently aggravate anemia and hemodilution and lead to severe maternal complications. This article is protected by copyright. All rights reserved.
- Enterovirus 71 outbreak in Northern Sydney, 2013: Case series and initial response. [Journal Article]
- J Paediatr Child Health 2014 Jul; 50(7):525-30.
Enteroviruses are a common cause of childhood disease which may manifest in a variety of ways. Enterovirus 71 (EV71) is a subtype of enterovirus which can cause meningoencephalomyelitis resulting in neurological sequelae including lethargy, weakness, ataxia, sleep myoclonus, urinary retention and, in severe cases, cardiorespiratory collapse due to neurogenic pulmonary oedema. EV71 was responsible for outbreaks in South East Asia in 1997-1998, in Western Australia in 1999 and in Sydney in 2000-2001. In 2013, we are experiencing another EV71 outbreak in Sydney. This study describes the discovery of a new outbreak in Sydney's Northern Beaches, the clinical findings as well as the public health response.Thirty-seven children in total presented with presumed EV71 to the Northern Beaches Health Service from December 2012 to April 2013. Most children presented with a prodrome lasting 2-7 days prior to seeking medical attention. Sleep myoclonus was a common presenting sign occurring in 65%. Neurological signs were subtle in the majority of children and were at times missed by clinicians on a child's first presentation. Forty-six per cent of children who presented to Northern Beaches Health Service during this outbreak required a transfer to a tertiary paediatric centre for more intensive care.The public health investigation was important in establishing that the disease was widespread throughout the community and not as a result to exposure to a single child care setting. Identification of risk factors enabled more targeted communication to medical practitioners, child care centres and parents within the local community.EV71 is in Australia and all clinicians seeing children in primary, secondary and tertiary care centres need to be aware of the disease, the subtle nature of initial symptoms and the potentially devastating consequences.
- Influenza causes prolonged disruption of the alveolar-capillary barrier in mice unresponsive to mesenchymal stem cell therapy. [JOURNAL ARTICLE]
- Am J Physiol Lung Cell Mol Physiol 2014 Jul 18.
Viral pneumonia is a major cause of acute respiratory distress syndrome (ARDS). Anti-inflammatory therapies for viral-induced lung injury show promise in preclinical models. Mesenchymal stem/stromal cells (MSCs) are multipotent, self-renewing cells that secrete anti-inflammatory cytokines and epithelial and endothelial growth factors. We inoculated mice intranasally with influenza A (murine-adapted PR8) or PBS, and sacrificed at multiple time points after infection for measures of lung injury and viral load. We report that influenza induces marked, long-lasting dysfunction of the alveolar-capillary barrier peaking at one week but lasting longer than 3 weeks post-infection. Weight loss, commonly employed as a criterion for euthanasia (and hence "survival") was found to be poorly predictive of the severity of lung injury at its peak; rather, persistent weight loss 11 days post-infection identified mice with impaired injury resolution. Murine and human bone-marrow derived MSCs (obtained from the NIH repository) were then administered intravenously during the rapid phase of injury progression. Murine MSCs (mMSCs) given twice 24 hours apart failed to improve weight loss, lung water, BAL inflammation, or histology. However, mMSCs prevented influenza-induced thrombocytosis and caused a modest reduction in lung viral load at day 7. Human MSCs administered intravenously showed a similar lack of efficacy. The results demonstrate that the influenza murine model bears important similarities to the slow resolution of ARDS in patients. Despite their potent therapeutic effects in many models of acute inflammation and lung injury, MSCs do not improve influenza-mediated lung injury in mice.
- Evaluation of Karl Storz CMAC Tip™ Device Versus Traditional Airway Suction in a Cadaver Model. [Journal Article]
- West J Emerg Med 2014 Jul; 15(4):548-53.
We compared the efficacy of Karl Storz CMAC Tip™ with inline suction to CMAC with traditional suction device in cadaveric models simulating difficult airways, using media mimicking pulmonary edema and vomit.This was a prospective, cohort study in which we invited emergency medicine faculty and residents to participate. Each participant intubated 2 cadavers (one with simulated pulmonary edema and one with simulated vomit), using CMAC with inline suction and CMAC with traditional suction. Thirty emergency medicine providers performed 4 total intubations each in a crossover trial comparing the CMAC with inline suction and CMAC with traditional suction. Two intubations were performed with simulated vomit and two with simulated pulmonary edema. The primary outcome was time to successful intubation; and the secondary outcome was proportion of successful intubation.The median time to successful intubation using the CMAC with inline suction versus traditional suction in the pulmonary edema group was 29s and 30s respectively (p=0.54). In the vomit simulation, the median time to successful intubation was 40s using the CMAC with inline suction and 41s using the CMAC with traditional suction (p=0.70). There were no significant differences in time to successful intubation between the 2 devices. Similarly, the proportions of successful intubation were also not statistically significant between the 2 devices. The proportions of successful intubations using the inline suction were 96.7% and 73.3%, for the pulmonary edema and vomit groups, respectively. Additionally using the handheld suction device, the proportions for the pulmonary edema and vomit group were 100% and 66.7%, respectively.CMAC with inline suction was no different than CMAC with traditional suction and was associated with no statistically significant differences in median time to intubation or proportion of successful intubations.
- [Death caused by heat stroke: case report]. [English Abstract, Journal Article]
- Srp Arh Celok Lek 2014 May-Jun; 142(5-6):360-4.
Heat stroke is the most dangerous among numerous disorders caused by elevated environmental temperature. It is characterized by an increased body temperature of over 40 degrees C, the dysfunction of the central nervous system and the development of multiple organ failure. The aim of this paper was to highlight problems in the clinical and post-mortal diagnosis of fatal heat stroke.A 20-year-old male was found unconscious on the street; on admission at the Emergency Center, Clinical Center of Serbia, Belgrade, he was in a coma. The body temperature of 40 degrees C was maintained despite the applied therapy, meningeal signs were negative, tachycardia with gallop rhythm, hypotension, bleeding from the nose and mouth, and presence of skin bruises. Laboratory findings: highly elevated LDH and creatine kinase, elevated serum creatinine, AST, and signs of DIC. Lethal outcome occurred 6 hours after admission, and the case remained clinically unsolved. Autopsy showed signs of hemorrhagic diathesis, brain and pulmonary edema, and microscopic examination revealed general congestion, internal bleeding in various organs, cerebral edema, massive blood aspiration and pulmonary edema. Toxicological and bacteriological examinations were negative. Based on these findings and subsequently obtained data on the conditions at the workplace where the young man had a part-time job, it was concluded that the violent death was caused by heat stroke.Since heat stroke is associated with a high mortality rate and high incidence of serious and permanent organ damage in survivors, it is important to make the diagnosis of heat stroke as quickly as possible and apply appropriate treatment. Misdiagnosis of heat stroke, and consequently inadequate treatment, with a potential fatal outcome for the patient, can be the reason for blaming doctors for the legal offense of medical malpractice in failing to administer first aid.
- Calcific embolization with infective endocarditis involving the posterior mitral leaflet in a patient with underlying hypertrophic obstructive cardiomyopathy. [JOURNAL ARTICLE]
- J Thromb Thrombolysis 2014 Jul 17.
We report a case of infective endocarditis (IE) involving the posterior mitral leaflet (PML) with calcific embolization in a patient with hypertrophic obstructive cardiomyopathy (HOCM). Amongst HOCM patients with IE, the anterior mitral leaflet and basal septal myocardium are almost always involved due to the endocardial damage caused by recurrent outflow obstruction and valvular regurgitation. The management of our patient was complicated by moderate mitral stenosis, repeated calcific embolic strokes, dynamic left ventricular outflow track obstruction, and respiratory failure due to flash pulmonary edema. To our knowledge, this is the first reported case of PML involvement in HOCM presenting in this manner.
- A Novel TNF-mediated Mechanism of Direct Epithelial Sodium Channel Activation. [JOURNAL ARTICLE]
- Am J Respir Crit Care Med 2014 Jul 16.
Rationale. Alveolar liquid clearance (ALC) is regulated by Na(+)-uptake through the apically expressed epithelial sodium channel (ENaC) and the basolaterally localized Na(+)-K(+)-ATPase in type II alveolar epithelial cells (AEC). Dysfunction of these Na(+) transporters during pulmonary inflammation can contribute to pulmonary edema. Objective. This study determined the precise mechanism by which the TIP peptide, mimicking the lectin-like domain of TNF, stimulates Na(+)-uptake in a homologous cell system in the presence or absence of the bacterial toxin pneumolysin (PLY). Methods. We used a combined biochemical, electrophysiological and molecular biological in vitro approach and assessed the physiological relevance of the lectin-like domain of TNF in ALC in vivo, by generating Triple mTNF knock-in (TKI) mice that express a mutant TNF with deficient Na(+)-uptake stimulatory activity. Measurements and Main Results. TIP peptide directly activates ENaC, but not the Na(+)-K(+)-ATPase, upon binding to the carboxy-terminal domain of the α subunit of the channel. In the presence of PLY, a mediator of pneumococcal-induced pulmonary edema, this binding stabilizes the ENaC-PIP2-MARCKS complex, necessary for the open probability conformation of the channel and preserves ENaC-α protein expression, by means of blunting the protein kinase C-α (PKC-α) pathway. TKI mice are more prone than wild type mice to develop edema with low dose intratracheal PLY, correlating with reduced pulmonary ENaC-α subunit expression. Conclusions. These results demonstrate a novel TNF-mediated mechanism of ENaC activation and indicate a physiological role for the lectin-like domain of TNF in the resolution of alveolar edema during inflammation.