Negative pressure pulmonary edema: a case report.

BACKGROUND: The negative pressure pulmonary edema is rare clinical situation which caused mainly by upper airway obstruction. However except upper airway obstruction, there may be other pathophysiological disorders making patients more vulnerable to pulmonary edema. Based on these disorders, upper airway obstruction is the trigger to induce negative pressure pulmonary edema. CASE PRESENTATION: This case was a 5-year-old girl with tumor on saddle area, her hormones level were abnormal preoperatively, such as cortisol, adrenocorticotrophic hormone, free T4 and total T4. During the stage of induction, negative pressure pulmonary edema took place due to mild upper airway obstruction. And the instant chest Computer tomography proved diagnosis clue. After intensive care, most lung field of this girl recovered to normal within 48 h. CONCLUSION: The patient with abnormal hormone levels is vulnerable to pulmonary edema, mild upper airway obstruction triggered negative pressure pulmonary. Thus pre-operation hormones supplement is as important as keeping upper airway unobstructed.

[Lung transplantation in patients with paraquat poisoning: a case report and literature review].

Objective: To analyze 8 cases of paraquat lung transplantation in the world, and to explore the timing of lung transplantation and the factors affecting prognosis. Methods: An analysis of the clinical data of a paraquat poisoning lung transplant patient completed by The 12th People's Hospital of Guangzhou Medical University and The First People's Hospital affiliated to Guangzhou Medical University in August 2017 and literature review. Results: A 26 years old female patient was admitted to the hospital ingested 20% paraquat solution 20ml. On the 58th day of poisoning, she underwent double lung transplantation under general anesthesia. The operation was successful. Excised lungs show extensive lung fibrosis in both lungs, which was consistent with paraquat poisoning. Used tacrolimus and corticosteroids and mycophenolate antirejection, the patient discharged 46 days after surgery. 7 articles were retrieved through the search tool, and a total of 8 articles included this case were reported. Five patients who underwent lung transplantation within 1 month after poisoning all died, And 3 patients conducted lung transplantation for more than 1 month after poisoning survived; Pathogenic bacteria were isolated from the sputum in 3 of the 8 cases, all containing Pseudomonas, 2 of which died, and our case survived. Conclusion: Appropriate transplantation time window is very important for the prognosis of paraquat poisoning after lung transplantation. Active treatment of the sputum pathogens, improving the donor receptor matching, and exhausting the various means to remove the paraquat from the storage pool which may improve success rate of lung transplantation.

Refractory Pulmonary Edema and Upper Body Hypoxemia During Veno-Arterial Extracorporeal Membrane Oxygenation-A Case for Atrial Septostomy.

Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) provides mechanical circulatory support for patients with advanced cardiogenic shock, facilitating myocardial recovery and limiting multi-organ failure. In patients with severely limited left ventricular ejection, peripheral VA-ECMO can further increase left ventricular and left atrial pressures (LAP). Failure to decompress the left heart under these circumstances can result in pulmonary edema and upper body hypoxemia, that is, myocardial and cerebral ischemia. Atrial septostomy can decrease LAP in these situations. However, the effects of atrial septostomy on upper body oxygenation remain unknown. After IRB approval, we identified 9 out of 242 adult VA-ECMO patients between January 2011 and June 2016 who also underwent atrial septostomy for refractory pulmonary edema/upper body hypoxemia. We analyzed LAP/pulmonary capillary wedge pressure (PCWP), right atrial pressures (RAPs), Pa O2 /Fi O2 ratios (blood samples from right radial artery), intrathoracic volume status, and resolution of pulmonary edema before and up to 48 h after septostomy. There were no procedure-related complications. Thirty-day survival was 44%. LAP/PCWP decreased by approximately 40% immediately following septostomy and remained so for at least 24 h. Pa O2 /Fi O2 ratios significantly increased from 0.49 (0.38-2.12) before to 5.35 (3.01-7.69) immediately after septostomy and continued so for 24 h, 6.6 (4.49-10.93). Radiographic measurements also indicated a significant improvement in thoracic intravascular volume status after atrial septostomy. Atrial septostomy reduces LAP and improves upper body oxygenation and intrathoracic vascular volume status in patients developing severe refractory pulmonary edema while undergoing peripheral VA-ECMO. Atrial septostomy therefore appears safe and suitable to reduce the risk of upper body ischemia under these circumstances.

TEVAR for Flash Pulmonary Edema Secondary to Thoracic Aortic Aneurysm to Pulmonary Artery Fistula.

Enlarging aneurysms in the thoracic aorta frequently remain asymptomatic. Fistulization of thoracic aortic aneurysms (TAA) to adjacent structures or the presence of a patent ductus arteriosus and TAA may lead to irreversible cardiopulmonary sequelae. This article reports on a large aneurysm of the thoracic aorta with communication to the pulmonary artery causing pulmonary edema and cardiorespiratory failure. The communication was ultimately closed after thoracic endovascular aortic aneurysm repair allowing rapid symptom resolution. Early diagnosis and closure of such communication in the presence of TAA are critical for prevention of permanent cardiopulmonary damage.

Neurogenic Pulmonary Edema in Aneurysmal Subarachnoid Hemorrhage.

Neurogenic pulmonary edema (NPE) is observed in cerebral injuries and has an impact on treatment results, being a predictor of fatal prognosis. In this study we retrospectively reviewed medical records of 250 consecutive patients with aneurysmal subarachnoid hemorrhage (SAH) for the frequency and treatment results of NPE. The following factors were taken under consideration: clinical status, aneurysm location, presence of NPE, intracranial pressure (ICP), and mortality. All patients had plain- and angio-computer tomography performed. NPE developed most frequently in case of the aneurysm located in the anterior communicating artery. The patients with grades I-III of SAH, according to the World Federation of Neurosurgeons staging, were immediately operated on, while those with poor grades IV and V had only an ICP sensor's implantation procedure performed. A hundred and eighty five patients (74.4 %) were admitted with grades I to III and 32 patients (12.8 %) were with grade IV and V each. NPE was not observed in SAH patients with grade I to III, but it developed in nine patients with grade IV and 11 patients with grade V. Of the 20 patients with NPE, 19 died. Of the 44 poor grade patients (grades IV-V) without NPE, 20 died. All poor grade patients had elevated ICP in a range of 24-56 mmHg. The patients with NPE had a greater ICP than those without NPE. Gender and age had no influence on the occurrence of NPE. We conclude that the development of neurogenic pulmonary edema in SAH patients with poor grades is a fatal prognostic as it about doubles the death rate to almost hundred percent.

Management of three cardiogenic pulmonary edemas occurring in a patient scheduled for left ventricular assist device implantation: indicators for determining left ventricular assist device pump speed.

A male patient with Marfan syndrome underwent aortic root replacement and developed left ventricular (LV) failure. Four years later, he underwent aortic arch and aortic valve replacement. Thereafter, his LV failure progressed, and cardiogenic pulmonary edema (CPE) appeared, which we treated with extracorporeal LV assist device (LVAD) placement. Three months later, the patient developed aspiration pneumonia, which caused hyperdynamic right ventricle (RV) and CPE. We treated by changing his pneumatic LVAD to a high-flow centrifugal pump. A month later, he underwent thoracoabdominal aortic replacement. After four weeks, he developed septic thrombosis and LVAD failure, which caused CPE. We treated with LVAD circuit replacement and an additional membrane oxygenator. Four months later, he underwent DuraHeart(®) implantation. During this course, pulmonary artery wedge pressure (PAWP) varied markedly. Additionally, systolic pulmonary artery pressure (sPAP), left atrial diameter (LAD), RV end-diastolic diameter (RVEDD) and estimated RV systolic pressure (esRVP) changed with PAWP changes. In this patient, LV failure and hyperdynamic RV caused the CPEs, which we treated by adjusting the LVAD output to the RV output. Determining LVAD output, RV function and LV end-diastolic diameter are typically referred, and PAWP, LAD, RVEDD, and sPAP could be also referred.

[A Case of Acute Pulmonary Edema after Open Abdominal Aortic Aneurysm Repair].

A 61-year-old man, who had previously undergone percutaneous coronary intervention (PCI) of the left anterior descending artery (LAD), was scheduled for open abdominal aortic aneurysm repair under general anesthesia. Although the left ventricular (LV) ejection fraction was 63%, diastolic dysfunction was identified (E/A 0.61). The patient received inhalation induction with 5% sevoflurane and an infusion of remifentanil (0.2µg · kg⁻¹ · min⁻¹). Rocuronium (0.6 mg · kg⁻¹) was administered and tracheal intubation was performed. Anesthesia was maintained with air-oxygen- sevoflurane, an infusion of remifentanil, and 700 µg fentanyl administered intravenously. An infusion of fentanyl (25 µg · hr⁻¹) in combination with rectus sheath block was administered for postoperative anal- gesia. Intraoperatively, we used arterial pressure-based cardiac output (CO), stroke volume variation (SVV), and transesophageal echocardiography as a guide for circulatory management The intraoperative net fluid in-out balance was 5,296 ml, and the duration of the procedure was 5.5 hr. The patient was extubated in the operating room because no significant findings were observed on the postoperative chest X-ray, and PaO2/FI02 (P/F) ratio was 405. At the termination of anesthesia, systolic blood pressure increased to 200 mmHg. The hypertension lasted until after extubation, following which SpO2 diminished gradually. And SpO2 was 78% and PaO2 was 56.7 Torr under 8 l of oxygen. A chest X-ray at this time showed pulmonary edema. There were no findings of ischemic heart disease on either ECG or echocardiography. Immediate vasodilator treatment for the hypertension and non-invasive posi- tive pressure ventilation for the hypoxia were commenced. The P/F ratio recovered to 240 by the night of the surgery, and a chest X-ray showed that the pul- monary edema had resolved. The patient was moved out of the ICU on the first day after the surgery. This case highlights the fact that even when LV systolic function is preserved, diastolic dysfunction may occur, leading to pulmonary congestion due to increased afterload.

[Reexpansion Pulmonary Edema during Emergency Surgery in a Patient with Spontaneous Hemopneumothorax].

A 43-year-old male patient with spontaneous hemopneumothorax of the right lung underwent emergency video-assisted thoracoscopic surgery for drainage, hemostasis and bullae resection. Fifteen minutes after reexpansion of the right lung, we found bubbly sputum coming out from the right tracheal tube and cloudy shadow in the right field of his chest X-ray. The occurrence of reexpansion pulmonary edema (RPE) was considered. Subsequent mechanical ventilation with PEEP and administration of steroid and diuretic was done as his treatment. His respiratory state was stabiized in the next two days. As the lung collapse following spontaneous hemopneumothorax often becomes more severe, we should pay attention to the occurrence of RPE after expansion of affected side lung. And, if it occurred, appropriate and prompt treatment as above should be done because of its high mortality.

Methylene blue attenuates ischemia--reperfusion injury in lung transplantation.

BACKGROUND: Ischemia-reperfusion injury (IRI) is one of the principal obstacles for the lung transplantation (LTx) success. Several strategies have been adopted to minimize the effects of IRI in lungs, including ex vivo conditioning of the grafts and the use of antioxidant drugs, such as methylene blue (MB). We hypothesized that MB could minimize the effects of IRI in a LTx rodent model. METHODS: Forty rats were divided into four groups (n = 10) according to treatment (saline solution or MB) and graft cold ischemic time (3 or 6 h). All animals underwent unilateral LTx. Recipients received 2 mL of saline or MB intraperitoneally before transplantation. After 2 h of reperfusion, arterial blood and exhaled nitric oxide samples were collected and bronchoalveolar lavage performed. Then animals were euthanized, and histopathology analysis as well as cell counts and cytokine levels measurements in bronchoalveolar lavage fluid were performed. RESULTS: There was a significant decrease in exhaled nitric oxide, neutrophils, interleukin-6, and tumor necrosis factor-α in MB-treated animals. PaO2 and uric acid levels were higher in MB group. CONCLUSIONS: MB was able in attenuating IRI in this LTx model.

Surgical treatment of chronic thromboembolic pulmonary hypertension.

It is likely that chronic thromboembolic pulmonary hypertension (CTEPH) is more prevalent than currently recognised. Imaging studies are fundamental to decision making with respect to operability. All patients with suspected CTEPH should be referred to an experienced surgical centre. Currently, there is no risk scoring stratification system to guide operability assessment and it is predominantly based on surgical experience. The aim of pulmonary endarterectomy (PEA) is the removal of obstructive material to immediately reduce pulmonary vascular resistance. PEA affords the best chance of cure, but is difficult to perfect. Recognition and clearance of distal segmental and subsegmental disease is the main problem. The basic surgical techniques include: median sternotomy incision, cardiopulmonary bypass, arteriotomy incisions within pericardium, and a true endarterectomy with meticulous full distal dissection. Deep hypothermic circulatory arrest is recommended as the best means of reducing blood flow in the pulmonary artery to allow a clear field for dissection. In the recent PEACOG (PEA and COGnition) trial there was no evidence of cognitive impairment post-PEA. Reperfusion pulmonary oedema and residual pulmonary hypertension are unique post-operative complications post-PEA and are associated with increased mortality. However, in-hospital mortality is now <5% in experienced centres.

Reverse cardiac remodelling and renal functional improvement following bilateral renal artery stenting for flash pulmonary oedema.

Acute flash pulmonary oedema (AFPO) is a life-threatening syndrome almost unique to patients with atheromatous renovascular disease (ARVD). Although recurrent AFPO is a widely accepted indication to consider renal revascularization, this is based on a number of case reports/series describing a successful outcome post-procedure. There is limited literature on the pathophysiological mechanisms and treatment effects of revascularization to support this clinical decision making. We report the case of a 65-year-old lady who presented with three episodes of AFPO. Investigations revealed severe bilateral renal artery stenosis. Post-revascularization, she experienced substantial improvement in energy levels and New York Heart Association class, with improvement in her blood pressure and renal function. Post-procedure, there were dramatic improvements in her cardiac morphology and function that were sustained at 1 year (ejection fraction improved from 39 to 65%, left ventricular mass decreased from 161 to 116 g) as well as renal function (isotopic glomerular filtration rate increased from 22.4 to 34.2 mL/min). This report provides new insights into the pathophysiological relationships between renal and cardiac changes in AFPO; the extent of the cardiac morphological changes was striking and unexpected.

Percutaneous balloon atrioseptostomy for left heart discharge in extracorporeal life support patients with persistent pulmonary edema.

AIMS: In severe myocardial dysfunction, extracorporeal life support (ECLS) can preserve organ perfusion. Occasionally, the high resulting afterload can lead to refractory pulmonary edema. We report our experience with percutaneous balloon atrioseptostomy used in this circumstance to discharge the left heart and prevent worsening pulmonary congestion. METHODS AND RESULTS: Between October 2002 and December 2009, 5 patients, with a mean age of 39 years, who were under peripheral ECLS underwent percutaneous balloon atrioseptostomy for refractory worsening pulmonary edema as determined by clinical, radiological, and echocardiographic criteria. Myocardial dysfunction was related to drug poisoning in 2 cases and to myocarditis in the 3 others. Atrioseptostomy successfully improved pulmonary edema and echocardiographic indices of left ventricular function in all cases. Four patients were eventually discharged. The fifth patient died in hospital due to multiorgan failure. CONCLUSIONS: In our experience, percutaneous balloon atrioseptostomy appeared to be a rapid, effective, and minimally invasive technique for offloading the left heart of patients with a reversible cardiac dysfunction under ECLS and suffering from refractory pulmonary edema.

Percutaneous mitral valve repair in a ventilator-dependant patient.

I report the case of a 57-year-old patient admitted to the intensive care unit with severe community-acquired pneumonia, complicated by prolonged mechanical ventilation of the lungs and intractable cardiac failure. He underwent percutaneous coronary angioplasty of the right coronary artery, but this did not improve his clinical condition. He was subsequently found to be suffering from mitral valve prolapse, that was felt to be the cause of recurrent episodes of severe pulmonary oedema. As open surgery was felt to be not feasible, the patient underwent percutaneous repair of his mitral valve using the MitraClip® device, and, after months of ventilatory support, was then weaned from the ventilator in a matter of days. While the procedure itself and the technology employed are still under evaluation, I conclude that the technique of percutaneous mitral valve repair may be considered for similar patients for whom open repair is contraindicated.

Renal artery intervention for a patient with flash pulmonary edema accompanied by elevation of troponin levels due to bilateral renal artery stenosis and multivessel coronary disease: a case report.

An 84-year-old woman complaining of acute-onset chest distress for 2 hours was referred to the Department of Cardiology, Guangzhou Red Cross Hospital, China. A physical examination showed signs of acute pulmonary edema with considerably elevated blood pressure of 186/120 mmHg. An electrocardiogram showed ST segment depression in leads I, II, and III, and from V4 to V6. A laboratory test showed markedly elevated creatine, high-sensitivity cardiac troponin T, and N-terminal pro-brain natriuretic peptide levels. Echocardiography showed a mildly enlarged left ventricle with an ejection fraction of 43%. The patient was diagnosed with acute coronary syndrome, non-ST segment elevation myocardial infarction, and Killip 3 grade heart function. The non-ST segment elevation myocardial infarction Global Registry of Acute Coronary Events score was 156. Emergency coronary angiography showed severe three-vessel disease with a global ejection fraction of 50% based on left ventricular angiography. Selective renal artery angiography was performed and major stenosis at the ostia in both renal arteries was found. We did not touch the coronary artery, but performed intervention of the renal artery by implanting two bare metal stents in both ostia of bilateral renal arteries. An unexpected clinical benefit was obtained.

Migration of a Kirschner wire to the heart in a Yorkshire terrier.

A 12-year-old, male Yorkshire terrier was presented for acute pulmonary oedema. Thoracic radiographs showed a linear metallic foreign body within the cardiac silhouette. Echocardiogram showed a hyperechoic line extending through the left ventricle, the mitral valve, leading into the left atrium. A 4 cm long Kirschner wire was surgically removed by left fourth thoracotomy. The dog died two days after surgery for acute pulmonary oedema. Necropsy showed thrombi on the mitral leaflets that impeded their movement.