Edema agudo de pulmón secundario a síndrome de absorción intravascular durante histeroscopia: a propósito de un caso / Acute pulmonary edema secondary to intravascular absorption syndrome during hysteroscopy: A case report

La histeroscopia es un procedimiento endoscópico que estudia el interior de la cavidad uterina y del canal endocervical con objetivo diagnóstico-terapéutico. Para obtener una visualización óptima de las estructuras se utilizan diversos fluidos como el suero salino fisiológico. Una complicación poco frecuente es la sobredosificación de volumen, lo cual puede asociarse a un síndrome de absorción intravascular tras histeroscopia, normalmente tras procedimientos largos o disección de tejidos. Respecto de este síndrome, no se disponen datos de incidencia y prevalencia, existiendo pocos casos reportados en relación a solución salina fisiológica. Se presenta el caso de una paciente sometida a resección miomatosa, que, como consecuencia del síndrome de absorción vascular, dio lugar a edema agudo de pulmón que requirió ingreso en la Unidad de Cuidados Intensivos.(AU)

Hysteroscopy is an exploratory endoscopic technique that studies the interior of the uterine cavity and the endocervical canal. Various fluids, such as physiological saline, are used to optimise visualisation of the internal structures during this procedure. A rare complication of hysteroscopy is fluid overload, which can be associated with intravascular absorption syndrome, usually after lengthy procedures or tissue dissection. There are no data on the incidence and prevalence of this syndrome, and few cases involving physiological saline solution have been reported. We present a case of hysteroscopic myomectomy complicated by vascular absorption syndrome, which gave rise to acute pulmonary oedema that required admission to the intensive care unit.(AU)

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.

[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.

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.

Creation of a restrictive atrial communication in heart failure with preserved and mid-range ejection fraction: effective palliation of left atrial hypertension and pulmonary congestion.

BACKGROUND: Left atrial decompression is considered in patients with symptomatic heart failure with preserved ejection fraction (HFpEF). We aimed to evaluate the feasibility and efficacy of transcatheter generation of a restrictive atrial septum communication to manage HFpEF from infancy to adulthood with cardiomyopathy and congenital heart defect. METHODS AND RESULTS: From June 2009 to December 2016, 24 patients (50% with an age less than 16 years) with HFpEF were palliated; NYHA-/Ross class IV (n = 10); median systemic ventricular ejection fraction 64 (range 35-78) %. Cardiomyopathy was classified as a restrictive (n = 4) or hypertrophic (n = 2). (75% related to congenital heart defects) Three patients had a systemic right ventricle; in the majority of patients, HFpEF was associated to complex congenital heart defects (n = 18). Mean pulmonary arterial pressures (PAP systolic/diastolic) were 56/28 (± 24/13), left atrial pressures (LAP, v-, a-wave, mean) 26/25/20 (± 7/10/6). Trans-septal puncture was used in 22 patients; foramen ovale dilatation in 2 patients. Median balloon size was 12 (range 6-18) mm; procedure time including diagnostic measures 125 (83-221) min. No procedural death or complications were observed. Mean LA-pressures decreased significantly to 19/19/15 ± 6/8/5 mmHg (p = 0.05); median brain natriuretic peptide (BNP) decreased from 392 (range 93-4401) pg/ml median BNP to 314 (range 61-1544) pg/ml (p = 0.05). Three patients died; one patient received orthotopic heart and one patient a heart-lung transplantation. No patient required so far an assist device. Clinical improvement occurred in all patients, in some after additional surgical or interventional approach. CONCLUSIONS: Transcatheter LA decompression is an age-independent, effective palliation treating patients with HFpEF.

Reconsideration of Neurogenic Pulmonary Edema as Source of Metastatic Cerebral Abscess Following Subarachnoid Hemorrhages: A Preliminary Study.

BACKGROUND: Subarachnoid hemorrhage (SAH) may be a cause of neurogenic pulmonary edema (NPE). It is well known that lymphatic fluid draining by thoracic duct to lungs consists of many dangerous metabolites, degraded tissue particles, and microbiologic pathogens. However, not enough studies have investigated whether NPE causes septicemia or not. In this study, we retrospectively examined our experimental materials to determine whether there is a meaningful relationship between NPE and cerebral abscess formation. METHODS: Forty-two rabbits were divided into 3 groups: Control (n = 5), SHAM (n = 7), and SAH (n = 30) with severe neurogenic lung edema detected in rabbits. The SHAM and SAH groups received 1 mL saline and 1 mL autologous arterial blood into the Sylvian cisterna, respectively. Weight, heartbeat, respiration rate, and blood pressure were recorded by routinely using monitoring devices. All multilevel lungs and brain tissue microsections were examined by stereologic and Cavalier methods. For statistical analysis, NPE criteria and the numbers of abscess or abscess resembling cores in the brains were estimated in all groups and compared. The Mann Whitney-U test was used to analyze the results statistically. RESULTS: All rabbits were around 4 years old; body weight was between 3.94 and 4.5 kg; normal heart rhythm rate was found between 251 ± 39/minutes and 281 ± 30/minutes; and respiration rate was between 24 ± 5/minutes and 36 ± 7/minutes. Histopathologic examinations showed that abscess formations frequently spread in middle cerebral arterial territories of all animals in the NPE-detected rabbits. While average abscess numbers were estimated as 3 ± 1 in 7 animals (n = 7; P < 0.005) in severe NPE-detected rabbits, only 1 ± 1 abscess core was detected in a less severe NPE that developed in 3 (n = 3; P < 0.05) animals. The vasospasm index values of pulmonary arteries (PAs) of all animals were 1.233 ± 0.065 in the control group; 1.567 ± 0.0430 in the SHAM group, and 2.890 ± 0.0453 in the SAH group (P < 0.05). CONCLUSIONS: This experimental study showed that NPE is a relatively common pathology following experimental SAH in rabbits. The NPE is frequently complicated with brain abscess as shown in this study. The pathophysiologic mechanism was concluded, as NPE may be responsible for cerebral abscess development via bacteria/cytotoxic particles conveyed by thoracic duct to lungs and transferred from the ruptured alveoli-capillary membrane to the brain by way of systemic circulation.

Effectiveness of Rescue Percutaneous Balloon Aortic Valvuloplasty in Patients With Severe Aortic Stenosis and Acute Heart Failure.

The prognosis of patients with cardiogenic shock (CS) or refractory pulmonary edema because of severe aortic stenosis remains poor. The purpose of this study was to assess the outcomes of rescue percutaneous balloon aortic valvuloplasty (PBAV) in the transcatheter aortic valve implantation (TAVI) era. Patients were consecutively included between 2008 and 2016. CS was defined as ≥1 sign of systemic hypoperfusion and need of catecholamines. Refractory pulmonary edema was defined as not controlled by optimal medical treatment. A total of 40 patients, 22 men (55%), aged 79 ± 9 years, were included: 17 with CS (42.5%), 23 with refractory pulmonary edema (57.5%). After PBAV, mean transaortic gradient decreased from 47 ± 16 mm Hg to 32 ± 10 mm Hg (p < 0.001), aortic valve area increased from 0.60 ± 0.18 cm2 to 0.88 ± 0.22 cm2 (p < 0.0001), left ventricular ejection fraction increased from 35 ± 15 to 37 ± 14% (p = 0.02), and systolic pulmonary artery pressure decreased from 61 ± 15 to 48 ± 12 mm Hg (p = 0.002). There was no procedural death. Early death occurred in 12 patients (30%). After PBAV, 16 of the 28 survivors (57%) were bridged to surgical aortic valve replacement (SAVR; n = 7) or TAVI (n = 9), and 12 (43%) were denied definitive therapy. The 2-year estimated survival rate was 71 ± 17% after SAVR, 36 ± 19% after TAVI, and 8 ± 8% after PBAV alone. In conclusion, rescue PBAV is safe in patients with CS and high-risk aortic stenosis or refractory pulmonary edema and may improve their dismal prognosis when followed by TAVI or SAVR.

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.

[Measurement of fractional flow reserve in patients with severe aortic stenosis: A valid test?] / Sténose aortique et lésions coronaires : la fractional flow reserve (FFR) est-elle valide ?

A 54-year-old woman was hospitalized for an acute pulmonary oedema revealing a severe aortic stenosis (AS) associated with an aortic aneurysm and a left ventricular hypertrophy (LVH). The coronary angiography found an equivocal left main lesion. Fractional flow reserve (FFR) showed hemodynamic significance (FFR=0.78) and optical coherence tomography confirmed this result with a minimal lumen area of 4.9mm2. FFR-guided percutaneous intervention is reported to improve outcome in patients with stable coronary disease. However, only few data are available in cases of AS. In this condition, secondary LVH is associated with microcirculatory dysfunction, which interferes with optimal hyperemia. An elevated right atrial pressure could also modify FFR measurement. This risk of underestimation of a coronary lesion in patients with severe AS has to be taken into consideration in clinical practice.

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.

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.