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Pulmonary Edema [keywords]
- Inducible nitric oxide synthase inhibition reverses pulmonary arterial dysfunction in lung transplantation. [JOURNAL ARTICLE]
- Inflamm Res 2014 Apr 24.
Ischemia-reperfusion injury (IRI) after lung transplantation remains a significant cause of morbidity and mortality. Lung IRI induces nitric oxide synthesis (iNOS) and reactive nitrogen species, decreasing nitric oxide bioavailability. We hypothesized that ischemia-induced iNOS intensifies with reperfusion and contributes to IRI-induced pulmonary arterial regulatory dysfunction, which may lead to early graft failure and cause pulmonary edema. The aim of this study was to determine whether ischemia-reperfusion alters inducible and endothelial nitric oxide synthase expression, potentially affecting pulmonary perfusion. We further evaluated the role of iNOS in post-transplantation pulmonary arterial disorder.We randomized 32 Sprague-Dawley rats into two groups. The control group was given a sham operation whilst the experimental group received orthotropic lung transplants with a modified three-cuff technique. Changes in lung iNOS, and endothelial nitric oxide synthase expression were measured after lung transplantation by enzyme-linked immunosorbent assay (ELISA). Vasoconstriction in response to exogenous phenylephrine and vasodilation in response to exogenous acetylcholine of pulmonary arterial rings were measured in vitro as a measure of vascular dysfunction. To elucidate the roles of iNOS in regulating vascular function, an iNOS activity inhibitor (N6-(1-iminoethyl)-L-lysine, L-NIL) was used to treat isolated arterial rings. In order to test whether iNOS inhibition has a therapeutic effect, we further used L-NIL to pre-treat transplanted lungs and then measured post-transplantation arterial responses.Lung transplantation caused upregulation of iNOS expression. This was also accompanied by suppression of both vasoconstriction and vasodilation of arterial rings from transplanted lungs. Removal of endothelium did not interfere with the contraction of pulmonary arterial rings from transplanted lungs. In contrast, iNOS inhibition rescued the vasoconstriction response to exogenous phenylephrine of pulmonary arterial rings from transplanted lungs. In addition, lung transplantation led to suppression of PaO2/FiO2 ratio, increased intrapulmonary shunt (Q s/Q t), and increase of lung wet to dry ratio (W/D), malondialdehyde and myeloperoxidase levels, all of which were reversed upon iNOS inhibition. Furthermore, inhibition of iNOS significantly rescued vascular function and alleviated edema and inflammatory cell infiltration in the transplanted lung.Our data suggest that lung transplantation causes upregulation of iNOS expression, and pulmonary vascular dysfunction. iNOS inhibition reverses the post-transplantational pulmonary vascular dysfunction.
- Right ventricular thrombus: a rare complication of ovarian hyperstimulation syndrome. [Journal Article]
- Int Cardiovasc Res J 2012 Dec; 6(4):131-2.
A 22 years old lady was admitted because of progressive dyspnea, severe abdominal protrusion and lower extremity edema. She had undergone ovarian hyperstimulation for primary infertility by Clomiphen and Human chorionic gonadotropin for 3 months. Abdominopelvic ultrasonography revealed bilateral enlarged multi cystic ovaries and massive ascites. Transesophageal echocardiography revealed a large thrombus in right ventrice apex. Spiral chest CT scan showed normal pulmonary vasculature with no evidence of pulmonary thromboembolism. Heparin was started and repeat echocardiographic study showed gradual disappearance of right ventricular thrombus. Human chorionic gonadotropin is the most important substance which leads to capillary leakage and fluid accumulation in third space. Fluid shift and hypovolemia may cause hypotension, hemoconcentration and formation of vascular thrombus.
- A complicated case of an immunocompetent patient with disseminated nocardiosis. [Journal Article]
- Infect Dis Rep 2014 Feb 18; 6(1):5327.
Nocardia species are aerobic, gram positive filamentous branching bacteria that have the potential to cause localized or disseminated infection. Nocardiosis is a rare disease that usually affects immunocompromised patients and presents as either pulmonary, cutaneous or disseminated nocardiosis. Forty-two year-old hispanic male presented to our care with bilateral lower extremity weakness, frontal headache, subjective fever, nausea, and vomiting. Brain computed tomography (CT) revealed multiple hyperdense lesions with vasogenic edema in the frontal, parietal and left temporal lobes. Chest CT demonstrated bilateral cavitary nodules in the lung and right hilar lymphadenopathy. Brain magnetic resonance imaging revealed multiple bilateral supratentorial and infratentorial rim enhancing lesions involving the subcortical gray-white matter interface with vasogenic edema. Patient was started on empiric therapy for unknown infectious etiology with no response. He eventually expired and autopsy findings revealed a right hilar lung abscess and multiple brain abscesses. Microscopic and culture findings from tissue sample during autopsy revealed nocardia wallacei species with multidrug resistance. The cause of death was stated as systemic nocadiosis (nocardia pneumonitis and encephalitis). The presence of simultaneous lung and brain abscesses is a reliable indication of an underlying Nocardia infection. An increased awareness of the various presentations of nocardiosis and a high index of clinical suspicion can help in a rapid diagnosis and improve survival in an otherwise fatal disease. This case highlights the importance of obtaining a tissue biopsy for definitive diagnosis on the initial presentation when an infectious process is considered in the differential diagnosis and early treatment can be initiated.
- Treatment of children with protein - losing enteropathy after fontan and other complex congenital heart disease procedures in condition with limited human and technical resources. [Journal Article]
- Mater Sociomed 2014 Feb; 26(1):39-42.
Protein-losing enteropathy (PLE) is a disorder characterized by abnormal and often profound enteric protein loss. It's relatively uncommon complication of Fontan and other complex congenital heart disease (CCHD) procedures. Because of the complexity and rarity of this disease process, the pathogenesis and pathophysiology of protein-losing enteropathy remain poorly understood, and attempts at treatment seldom yield long-term success.is to describe single centre experience in diagnosis, evaluation, management and treatment of children with protein-losing enteropathy after Fontan and other CCHD procedures in the current era and in centre with limited human and technical resources, follows with a comprehensive review of protein-losing enteropathy publications, and concludes with suggestions for prevention and treatment.Retrospectively we analyzed patients with CCHD and protein-losing enteropathy in our institution, starting from January 2000 to December 2012. The including criteria were age between two and 17 years, to have a complex congenital heart disease and available complete documentation of cardiac surgery under cardiopulmonary bypass.Of all patients we evaluated 18 cases with protein-losing enteropathy, aged 6 to 19 years (mean 14±9); there were three children who had undergone screening procedure for D-transposition, one Tetralogy of Fallot, and remaining 14 patients had undergone Fontan procedures; (anatomic diagnosis are: six with tricuspid atresia, seven with d-transposition, double outlet right ventricle and pulmonary atresia and two with hypoplastic left heart syndrome). The diagnosis of protein-losing enteropathy was made at median age of 5.6 years, ranging from 13 months to 15 years. Diagnosis was made using alpha 1-antitrypsin as a gold marker in stool. By physical examination in 14 patients edema was found, in three ascites, and six patients had pleural effusion. Laboratory findings at the time of diagnosis are: abnormal enteric protein loss was documented at the time of diagnosis in all 18 patients. At the time of diagnosis all patients receiving some form of anticoagulation, 17 patients receiving other medication: 17 - diuretics and ACE inhibitors, 12 digoxin, 9 antiarrhytmics. Cross-sectional echocardiography was performed for all patients and different abnormalities were registered. In 14 patients also magnetic resonance was performed. Therapeutic approach was based on the non-specific medication (diet, diuretics, digoxin, ACE inhibitors, and anticoagulants), heparin and corticosteroids therapy. Long-term response to this type of therapy was registered in three patients. Nine patients underwent treatment with heparin and corticosteroids and no one experienced long term benefit. Despite of needs for catheter therapy or surgical intervention in our study, in the absent of technical and human resources now any one had underwent those procedures. Six patients has been transferred abroad and in five of them surgical intervention was perform.Protein-losing enteropathy remains a devastating complication of Fontan procedure and despite in advantages in surgical and medical therapy there is no evidence that protein-losing enteropathy is less common in the current area.
- Clinical presentation of hypertensive crises in emergency medical services. [Journal Article]
- Mater Sociomed 2014 Feb; 26(1):12-6.
The objective of this study is to evaluate the incidence and clinical presentation of hypertensive crises in the Emergency medical services of the Community Health Centre "Dr. Mustafa Šehović" Tuzla in relation to age, sex, duration and severity of hypertension, as well as the prevalence of accompanying symptoms and clinical manifestations.The study was conducted between November 2009 and April 2010 and included 180 subjects of both sexes, aged 30-80 with a diagnosis of arterial hypertension. All subjects were divided into two groups: a control group, which consisted of subjects without hypertensive crisis (95 subjects) and an experimental group that consisted of subjects with hypertensive crisis (85 subjects).The study results indicate that female subjects were significantly over- represented compared to men (60% vs. 40 %, p=0.007). The average age of the male subjects was 55.83±11.06 years, while the female subjects' average age was 59.41±11.97 years. The incidence of hypertensive crisis was 47.22%, with hypertensive urgency significantly more represented than emergency (16.47% vs. 83.53%, p<0.0001). The majority of subjects in the experimental group (28.23%) belonged to the age group of 60-69 years of age: 26.76% urgency and 35.71% emergency. The most common accompanying symptoms in hypertensive subjects were headache (75%), chest pain (48.33%), vertigo (44.44%), shortness of breath (38.88%) and nausea (33.89%). The most common symptoms in subjects with hypertensive crisis were headache (74.11%), chest pain and shortness of breath (62.35%), vertigo (49.41%), and nausea and vomiting (41.17%).Chest pain, shortness of breath, nausea and vomiting were significantly over-represented in subjects with hypertensive crisis (p<0.005). Clinical manifestations of hypertensive emergencies in almost all subjects included acute coronary syndrome, and only one subject had acute pulmonary edema.
- Twin Infant with Lymphatic Dysplasia Diagnosed with Noonan Syndrome by Molecular Genetic Testing. [JOURNAL ARTICLE]
- Fetal Pediatr Pathol 2014 Apr 22.
Noonan Syndrome is an autosomal dominant disorder characterized by short stature, congenital heart defects, developmental delay, dysmorphic facial features and occasional lymphatic dysplasias. The features of Noonan Syndrome change with age and have variable expression. The diagnosis has historically been based on clinical grounds. We describe a child that was born with congenital refractory chylothorax and subcutaneous edema suspected to be secondary to pulmonary lymphangiectasis. The infant died of respiratory failure and anasarca at 80 days. The autopsy confirmed lymphatic dysplasia in lungs and mesentery. The baby had no dysmorphic facial features and was diagnosed postmortem with Noonan syndrome by genomic DNA sequence analysis as he had a heterozygous mutation for G503R in the PTPN11 gene.
- The predictive Value of Total Neutrophil Count and Neutrophil/Lymphocyte Ratio in Predicting In-hospital Mortality and Complications after STEMI. [Journal Article]
- J Cardiovasc Thorac Res 2014; 6(1):35-41.
Introduction: Leukocytosis, predominantly neutrophilia, has previously been described following ST elevation myocardial infarction (STEMI). The exact contribution of this phenomenon to the clinical outcome of STEMI is yet to be shown. We examined cellular inflammatory response to STEMI in the blood and its association with in-hospital mortality and/or adverse clinical events.
Methods:In this cross-sectional study, 404 patients who were admitted with the diagnosis of acute STEMI at Madani Heart Hospital from March 2010 to March 2012 were studied. The complete blood cell count (CBC) was obtained from all patientswithin12-24 hours of the onset of symptoms. Total leukocytes were counted and differential count was obtained for neutrophils, lymphocytes and neutrophil/lymphocyte ratio (NLR) were evaluated. Association of cellular response with the incidence of post-MI mortality/complications was assessed by multiple logistic regression analyses.
Results:In-hospital mortality and post-STEMI complication rate were 3.7% and 43.6%, respectively. Higher age (P=0.04), female gender (0.002), lower ejection fraction (P<0.001) and absolute neutrophil count (P=0.04) were predictors of mortality. Pump failure in the form of acute pulmonary edema or cardiogenic shock occurred in 35 (8.9%) of patients. Higher leukocyte (P<0.03) and neutrophil counts (P<0.03) and higher NLR (P=0.01) were predictors of failure. The frequency of ventricular tachyarrhythmias (VT/VF) at the first day was associated with higher neutrophil count (P<0.001) and higher NLR level (P<0.001). In multivariate analysis neutrophil count was an independent predictor of mortality (OR=2.94; 1.1-8.4, P=0.04), and neutrophil count [OR=1.1, CI (1.01-1.20), P=0.02], female gender [OR=2.34, CI (1.02-4.88), P=0.04] and diabetes [OR=2.52, CI (1.21-5.2), P=0.003] were independent predictors of heart failure.
Conclusion:A single CBC analysis may help to identify STEMI patients at risk for mortality and heart failure, and total neutrophil count is the most valuable in predicting both.
- Percutaneous minimally-invasive fetoscopic surgery for spina bifida aperta - Part II Maternal management and outcome. [JOURNAL ARTICLE]
- Ultrasound Obstet Gynecol 2014 Apr 21.
Minimally-invasive fetoscopic surgery of spina bifida aperta aims at improving postnatal neurological outcome of affected fetuses. The objective of this retrospective study was to assess maternal morbidity and outcome of this procedure in 51 women that were operated at a mean gestational age of 24 weeks at our center between July 2010 and June 2013.We studied our charts for the peri- and postoperative occurrence of maternal death, need for maternal blood transfusion, placental abruption, pulmonary edema, spontaneous labor, oligohydramnios, chorioamnionitis, chorioamniotic membrane separation, length of hospitalization, amniotic fluid leakage, gestational age at delivery and status of hysterotomy site.In all 51 women, maternal demise, placental abruption or the need for maternal blood transfusion were not observed in the perioperative period. Chorioamniotic membrane separation occurred in two, postoperative uterine contractions in one, mild pulmonary edema in one, and oligohydramnios in seven patients. One patient developed chorioamnionitis one week after fetal surgery; the fetus from this patient died from prematurity. All other babies survived gestation. Amniotic fluid leakage occurred in 43 patients at a mean gestational age of 29.7 (range 22.6-37.3) weeks; two of these patients developed chorioamnionitis. Length of hospitalization after surgery was 7.2 (range 4-12) days. Mean gestational age at delivery was 33 (range 24.6-38.1) weeks. All abdominal and uterine trocar insertion sites were well healed.Minimally-invasive fetoscopic surgery for spina bifida aperta was safe for most maternal patients. Despite the common occurrence of amniotic leakage the majority now delivers well beyond 32 weeks of gestation.
- Case report: pulmonary edema induced by breath holding in an adolescent patient. [Journal Article]
- AACN Adv Crit Care 2014 Apr-Jun; 25(2):101-3.
- [Case of successful thrombolytic therapy use in complex cardio-pulmonary resuscitation for massive pulmonary thromboembolism in parturient after elective caesarian operation]. [English Abstract, Journal Article]
- Anesteziol Reanimatol 2013 Nov-Dec; (6):54-6.
Pulmonary thromboembolism is a main cause of parturient mortality in the world. Recently there are few reports about a thrombolytic therapy use in parturient in medical publications. The article deals with a case of successful application of thrombolysis in a complex cardio-pulmonary resuscitation in parturient with massive pulmonary thromboembolism. Unexpected dyspnea and hypotension occurred in the 30 years old woman after elective caesarian operation. Syndrome S1-Q3 was fixed on an ECG monitor. Cardiac arrest was fixed in 10 minutes later. Streptokinase was administrated in a 1 hour after beginning of the resuscitation. Haemodynamic parameters recovered almost after the administration of streptokinase. Severe uterine bleeding occurred in 20 minutes after the administration. Uterine extirpation and tight tamponade of the small pelvis was performed for the bleeding stopping. Later a floating thrombus was diagnosed in the right femoral vein. Tromboectomy was performed. Convulsions had place on first and second day after the resuscitation. Cerebral edema was diagnosed by computed tomography. Consciousness occurred on the fourth day and the woman was weaned from the ventilator on the fifth day. The patient was discharged from the hospital on 20th day without neurological complications.