Severe Respiratory Failure Developing in the Course of High-Altitude Pulmonary Edema in an Alpinist with COVID-19 Pneumonia: A Case Report.

Pigon, Katarzyna, Ryszard Grzanka, Ewa Nowalany-Kozielska, and Andrzej Tomasik. Severe respiratory failure developing in the course of high-altitude pulmonary edema in an alpinist with COVID-19 pneumonia: a case report. High Alt Med Biol. 23:372-376, 2022.-The case of a 38-year-old Polish alpinist, evacuated from base camp (4,200 m) under Lenin's Peak due to severe high-altitude pulmonary edema (HAPE) and symptoms of acute mountain sickness/high-altitude cerebral edema (HACE), is presented. Starting the expedition, the man was asymptomatic and had a negative COVID-19 molecular test. After a few days of trekking, he developed typical HAPE and HACE. After evacuation to the hospital in Bishkek, a diagnosis of acute bronchopneumonia was made by computed tomography (CT) imaging. A COVID-19 test was not performed at that time. After returning to Poland, a complete noninvasive cardiac and pulmonary assessment disclosed no pathology. The initial chest CT reassessment was read as demonstrating the densities typical for COVID-19 pneumonia, and a SARS-CoV-2 antibody test corroborated the diagnosis. Pre-existing lung disease increases the risk of developing HAPE. In the era of the COVID-19 pandemic, people traveling at a high altitude and unaware of the infection are at particular risk.

Negative-pressure pulmonary edema after mammoplasty: a case report.

Negative-pressure pulmonary edema (NPPE) is a rare but life-threatening postoperative complication that occurs due to the acute obstruction of the upper airway. In our case report, we present a 25-year-old female patient who underwent elective mammoplasty under general anesthesia and developed NPPE 4 hours after extubation. The patient had a preoperative mallampati score of 3. After routine anesthesia induction, the patient was intubated with an endotracheal tube with a guide wire. Aspiration wasn't observed during extubation. The patient was followed in the post-anesthesia care unit (PACU) for 30 minutes with a saturation of 95% and was subsequently transferred to the service. Four hours after the operation, the patient was re-examined due to dyspnea and shortness of breath. Due to oxygen saturation of 88% and pO2of 56mmHg despite mask ventilation, the patient was admitted to the intensive care unit (ICU). A computed tomography (CT) scan revealed extensive diffuse ground-glass opacities and consolidations in both lungs. She did not respond to mask ventilation and was given non-invasive ventilation with continuous positive airway pressure (CPAP). Forced diuresis was induced with furosemide. Tachypnea resolved within 2 hours after CPAP was initiated, the patient did not require oxygen support and COVID-19 polymerase chain reaction (PCR) testing was negative. Subsequently, the patient was discharged to the clinical ward on postoperative day 1. When considering NPPE, early diagnosis and respiratory support are associated with reduced mortality and rapid recovery. Patients who develop laryngospasm during extubation must be closely monitored, and in the case of pulmonary edema, NPPE should be considered in the differential diagnosis.

Severe acute reentry high altitude pulmonary edema in pediatric patients: report of three cases and literature review.

BACKGROUND: High Altitude Pulmonary Edema (HAPE) is a fatal form of severe high-altitude illness. It is a form of noncardiogenic, noninfectious pulmonary edema secondary to alveolar hypoxia. The exact incidence of HAPE in children is unknown; however, most literature reports an incidence between 0.5-15%. There are three proposed HAPE types including classic HAPE, reentry HAPE, and high-altitude resident pulmonary edema (HARPE). CASE: We present three pediatric patients who were diagnosed with re-entry high altitude pulmonary edema and did not have any underlying cardiac abnormalities. All patients reside in areas of high altitude with a history of travelling to places of lower altitude. They had respiratory infections prior to the manifestation of HAPE. CONCLUSIONS: These are the first reported cases of children with reentry HAPE in Saudi Arabia. Reentry HAPE can occur in otherwise healthy children. Rapid ascent to high altitude and recent respiratory infections are the most commonly reported triggers. Prognosis is very favorable with a very rapid response to oxygen therapy. Education about HAPE is mandatory for families and health care workers working in high altitude areas.

Utility of a Pulmonary Oedema Score for Predicting the Need for Mechanical Ventilation in COVID-19 Patients in a General Hospital.

BACKGROUND: The Radiographic Assessment of Lung Edema (RALE) score has been used to estimate the extent of pulmonary damage in patients with acute respiratory distress syndrome and might be useful in patients with COVID-19. AIM OF THE STUDY: To examine factors associated with the need for mechanical ventilation in hospitalized patients with a clinical diagnosis of COVID-19, and to estimate the predictive value of the RALE score. METHODS: In a series of patients admitted between April 14 and August 28, 2020, with a clinical diagnosis of COVID-19, we assessed lung involvement on the chest radiograph using the RALE score. We examined factors associated with the need for mechanical ventilation in bivariate and multivariate analysis. The area under the receiver operating curve (AUC) indicated the predictive value of the RALE score for need for mechanical ventilation. RESULTS: Among 189 patients, 90 (48%) were judged to need mechanical ventilation, although only 60 were placed on a ventilator. The factors associated with the need for mechanical ventilation were a RALE score >6 points, age >50 years, and presence of chronic kidney disease. The AUC for the RALE score was 60.9% (95% CI 52.9-68.9), indicating it was an acceptable predictor of needing mechanical ventilation. CONCLUSIONS: A score for extent of pulmonary oedema on the plain chest radiograph was a useful predictor of the need for mechanical ventilation of hospitalized patients with COVID-19.

Acute respiratory distress syndrome.

ABSTRACT: Acute respiratory distress syndrome (ARDS) is a severe, often fatal, lung condition frequently seen in patients in the ICU. ARDS is triggered by an inciting event such as pneumonia or sepsis, which is followed by an inappropriate host inflammatory response that results in pulmonary edema and impaired gas exchange, and may progress to fibrosis. With the increased spotlight and discussion focused on ARDS during the COVID-19 pandemic, healthcare providers must be able to identify and manage symptoms based on evidence-based research.

Safety and preliminary efficacy of sequential multiple ascending doses of solnatide to treat pulmonary permeability edema in patients with moderate to severe ARDS in a randomized, placebo-controlled, double-blind trial: preliminary evaluation of safety and feasibility in light of the COVID-19 pandemic.

BACKGROUND: In May 2018, the first patient was enrolled in the phase-IIb clinical trial "Safety and Preliminary Efficacy of Sequential Multiple Ascending Doses of Solnatide to Treat Pulmonary Permeability Edema in Patients with Moderate to Severe ARDS." With the onset of the COVID-19 pandemic in early 2020, the continuation and successful execution of this clinical study was in danger. Therefore, before the Data Safety Monitoring Board (DSMB) allowed proceeding with the study and enrollment of further COVID-19 ARDS patients into it, additional assessment on possible study bias was considered mandatory. METHODS: We conducted an ad hoc interim analysis of 16 patients (5 COVID-19- ARDS patients and 11 with ARDS from different causes) from the phase-IIB clinical trial. We assessed possible differences in clinical characteristics of the ARDS patients and the impact of the pandemic on study execution. RESULTS: COVID-19 patients seemed to be less sick at baseline, which also showed in higher survival rates over the 28-day observation period. Trial specific outcomes regarding pulmonary edema and ventilation parameters did not differ between the groups, nor did more general indicators of (pulmonary) sepsis like oxygenation ratio and required noradrenaline doses. CONCLUSION: The DSMB and the investigators did not find any evidence that patients suffering from ARDS due to SARS-CoV-2 may be at higher (or generally altered) risk when included in the trial, nor were there indications that those patients might influence the integrity of the study data altogether. For this reason, a continuation of the phase IIB clinical study activities can be justified. Researchers continuing clinical trials during the pandemic should always be aware that the exceptional circumstances may alter study results and therefore adaptations of the study design might be necessary.

An antagonist of growth hormone-releasing hormone protects against LPS-induced increase of bronchoalveolar lavage fluid protein concentration.

Growth Hormone-Releasing Hormone (GHRH) is a neuropeptide regulating the release of Growth Hormone (GH) from the anterior pituitary gland, and acts as a growth factor in a diverse variety of tissues. GHRH antagonists (GHRHAnt) have been developed to counteract those events, and the beneficial effects of those peptides toward homeostasis have been associated with anti-inflammatory activities. Our lab is interested in delineating the mechanisms governing endothelial barrier function. Our goal is to establish new grounds on the development of efficient countermeasures against Acute Respiratory Distress Syndrome (ARDS), which has been associated with thousands of deaths worldwide due to COVID-19. Herein we demonstrate in vivo that GHRHAnt suppresses LPS-induced increase in bronchoalveolar lavage fluid (BALF) protein concentration, thus protecting the lungs against edema and inflammation.

What is the impact of microvascular complications of diabetes on severe COVID-19?

Evidence suggests severe coronavirus disease-19 (COVID-19) infection is characterised by pulmonary and systemic microvasculature dysfunction, specifically, acute endothelial injury, hypercoagulation and increased capillary permeability. Diabetes, which is also characterised by vascular injury in itself, confers an increased risk of adverse COVID-19 outcomes. It has been suggested that pre-existing endothelial dysfunction and microvascular disease in diabetes will exacerbate the vascular insults associated with COVID-19 and thus lead to increased severity of COVID-19 infection. In this article, we evaluate the current evidence exploring the impact of microvascular complications, in the form of diabetic retinopathy and nephropathy, in individuals with COVID-19 and diabetes. Future insights gained from exploring the microvascular injury patterns and clinical outcomes may come to influence care delivery algorithms for either of these conditions.

Re-expansion pulmonary edema following a pneumothorax drainage in a patient with COVID-19.

BACKGROUND: Re-expansion pulmonary edema is an uncommon complication following drainage of a pneumothorax or pleural effusion. While pneumothorax is noted to complicate COVID-19 patients, no case of COVID-19 developing re-expansion pulmonary edema has been reported. CASE REPRESENTATION: A man in his early 40 s without a smoking history and underlying pulmonary diseases suddenly complained of left chest pain with dyspnea 1 day after being diagnosed with COVID-19. Chest X-ray revealed pneumothorax in the left lung field, and a chest tube was inserted into the intrathoracic space without negative pressure 9 h after the onset of chest pain, resulting in the disappearance of respiratory symptoms; however, 2 h thereafter, dyspnea recurred with lower oxygenation status. Chest X-ray revealed improvement of collapse but extensive infiltration in the expanded lung. Therefore, the patient was diagnosed with re-expansion pulmonary edema, and his dyspnea and oxygenation status gradually improved without any intervention, such as steroid administration. Abnormal lung images also gradually improved within several days. CONCLUSIONS: This case highlights the rare presentation of re-expansion pulmonary edema following pneumothorax drainage in a patient with COVID-19, which recovered without requiring treatment for viral pneumonia. Differentiating re-expansion pulmonary edema from viral pneumonia is crucial to prevent unnecessary medication for COVID-19 pneumonia and pneumothorax.

The Oxygen Transport Triad in High-Altitude Pulmonary Edema: A Perspective from the High Andes.

Acute high-altitude illnesses are of great concern for physicians and people traveling to high altitude. Our recent article "Acute Mountain Sickness, High-Altitude Pulmonary Edema and High-Altitude Cerebral Edema, a View from the High Andes" was questioned by some sea-level high-altitude experts. As a result of this, we answer some observations and further explain our opinion on these diseases. High-Altitude Pulmonary Edema (HAPE) can be better understood through the Oxygen Transport Triad, which involves the pneumo-dynamic pump (ventilation), the hemo-dynamic pump (heart and circulation), and hemoglobin. The two pumps are the first physiologic response upon initial exposure to hypobaric hypoxia. Hemoglobin is the balancing energy-saving time-evolving equilibrating factor. The acid-base balance must be adequately interpreted using the high-altitude Van Slyke correction factors. Pulse-oximetry measurements during breath-holding at high altitude allow for the evaluation of high altitude diseases. The Tolerance to Hypoxia Formula shows that, paradoxically, the higher the altitude, the more tolerance to hypoxia. In order to survive, all organisms adapt physiologically and optimally to the high-altitude environment, and there cannot be any "loss of adaptation". A favorable evolution in HAPE and pulmonary hypertension can result from the oxygen treatment along with other measures.

Severe acute mitral valve regurgitation in a COVID-19-infected patient.

The ongoing SARS-CoV-2 (COVID-19) pandemic has presented many difficult and unique challenges to the medical community. We describe a case of a middle-aged COVID-19-positive man who presented with pulmonary oedema and acute respiratory failure. He was initially diagnosed with acute respiratory distress syndrome. Later in the hospital course, his pulmonary oedema and respiratory failure worsened as result of severe acute mitral valve regurgitation secondary to direct valvular damage from COVID-19 infection. The patient underwent emergent surgical mitral valve replacement. Pathological evaluation of the damaged valve was confirmed to be secondary to COVID-19 infection. The histopathological findings were consistent with prior cardiopulmonary autopsy sections of patients with COVID-19 described in the literature as well as proposed theories regarding ACE2 receptor activity. This case highlights the potential of SARS-CoV-2 causing direct mitral valve damage resulting in severe mitral valve insufficiency with subsequent pulmonary oedema and respiratory failure.

Differential Diagnosis of Negative Pressure Pulmonary Edema During COVID-19 Pandemic.

ABSTRACT: Negative pressure pulmonary edema (NPPE) is a form of noncardiogenic pulmonary edema that typically occurs in response to an upper airway obstruction, where patients generate high negative intrathoracic pressures, leading to a pulmonary edema especially in the postoperative period. Here, we report a case of NPPE following general anesthesia that can easily be misdiagnosed as COVID-19 both radiologically and clinically during this pandemic. Twenty-year-old male was presented with sudden onset respiratory distress, tachypnea, and cyanosis just after the rhinoplasty surgery under general anesthesia. Chest radiography and thoracic computed tomography scans revealed the bilateral patchy alveolar opacities with decreased vascular clarity that looks similar to COVID-19 radiology. Negative pressure pulmonary edema is a sudden onset and life-threatening complication following general anesthesia particularly after head and neck surgery in young healthy individuals. It is a clinical condition that cannot be diagnosed unless it comes to mind. While both NPPE and COVID-19 cause hypoxemia and respiratory distress, as well as ground-glass opacities in the chest computed tomography, those opacities in NPPE appear mostly in central areas, whereas those opacities are mostly seen in peripheral areas in COVID-19. Furthermore, while NPPE cause decreased vascular clarity, COVID-19 causes vascular dilatations in the areas of opacities. Those differences together with medical history of the patient is crucial to differentiate these 2 similar identities. Negative pressure pulmonary edema requires an immediate recognition and intervention, therefore, we would like to raise the awareness of clinicians for such condition to avoid possible mistakes during the pandemic situation.

Haemodynamic monitoring and management in COVID-19 intensive care patients: an International survey.

PURPOSE: To survey haemodynamic monitoring and management practices in intensive care patients with the coronavirus disease 2019 (COVID-19). METHODS: A questionnaire was shared on social networks or via email by the authors and by Anaesthesia and/or Critical Care societies from France, Switzerland, Belgium, Brazil, and Portugal. Intensivists and anaesthetists involved in COVID-19 ICU care were invited to answer 14 questions about haemodynamic monitoring and management. RESULTS: Globally, 1000 questionnaires were available for analysis. Responses came mainly from Europe (n = 460) and America (n = 434). According to a majority of respondents, COVID-19 ICU patients frequently or very frequently received continuous vasopressor support (56%) and had an echocardiography performed (54%). Echocardiography revealed a normal cardiac function, a hyperdynamic state (43%), hypovolaemia (22%), a left ventricular dysfunction (21%) and a right ventricular dilation (20%). Fluid responsiveness was frequently assessed (84%), mainly using echo (62%), and cardiac output was measured in 69%, mostly with echo as well (53%). Venous oxygen saturation was frequently measured (79%), mostly from a CVC blood sample (94%). Tissue perfusion was assessed biologically (93%) and clinically (63%). Pulmonary oedema was detected and quantified mainly using echo (67%) and chest X-ray (61%). CONCLUSION: Our survey confirms that vasopressor support is not uncommon in COVID-19 ICU patients and suggests that different haemodynamic phenotypes may be observed. Ultrasounds were used by many respondents, to assess cardiac function but also to predict fluid responsiveness and quantify pulmonary oedema. Although we observed regional differences, current international guidelines were followed by most respondents.

[Position Paper for the State of the Art Application of Respiratory Support in Patients with COVID-19 - German Respiratory Society]. / Positionspapier zur praktischen Umsetzung der apparativen Differenzialtherapie der akuten respiratorischen Insuffizienz bei COVID-19.

Against the background of the pandemic caused by infection with the SARS-CoV-2, the German Society for Pneumology and Respiratory Medicine (DGP e.V.), in cooperation with other associations, has designated a team of experts in order to answer the currently pressing questions about therapy strategies in dealing with COVID-19 patients suffering from acute respiratory insufficiency (ARI).The position paper is based on the current knowledge that is evolving daily. Many of the published and cited studies require further review, also because many of them did not undergo standard review processes.Therefore, this position paper is also subject to a continuous review process and will be further developed in cooperation with the other professional societies.This position paper is structured into the following five topics:1. Pathophysiology of acute respiratory insufficiency in patients without immunity infected with SARS-CoV-22. Temporal course and prognosis of acute respiratory insufficiency during the course of the disease3. Oxygen insufflation, high-flow oxygen, non-invasive ventilation and invasive ventilation with special consideration of infectious aerosol formation4. Non-invasive ventilation in ARI5. Supply continuum for the treatment of ARIKey points have been highlighted as core statements and significant observations. Regarding the pathophysiological aspects of acute respiratory insufficiency (ARI), the pulmonary infection with SARS-CoV-2 COVID-19 runs through three phases: early infection, pulmonary manifestation and severe hyperinflammatory phase.There are differences between advanced COVID-19-induced lung damage and those changes seen in Acute Respiratory Distress Syndromes (ARDS) as defined by the Berlin criteria. In a pathophysiologically plausible - but currently not yet histopathologically substantiated - model, two types (L-type and H-type) are distinguished, which correspond to an early and late phase. This distinction can be taken into consideration in the differential instrumentation in the therapy of ARI.The assessment of the extent of ARI should be carried out by an arterial or capillary blood gas analysis under room air conditions and must include the calculation of the oxygen supply (measured from the variables of oxygen saturation, the Hb value, the corrected values of the Hüfner number and the cardiac output). In principle, aerosols can cause transmission of infectious viral particles. Open systems or leakage systems (so-called vented masks) can prevent the release of respirable particles. Procedures in which the invasive ventilation system must be opened, and endotracheal intubation must be carried out are associated with an increased risk of infection.The protection of personnel with personal protective equipment should have very high priority because fear of contagion must not be a primary reason for intubation. If the specifications for protective equipment (eye protection, FFP2 or FFP-3 mask, gown) are adhered to, inhalation therapy, nasal high-flow (NHF) therapy, CPAP therapy or NIV can be carried out according to the current state of knowledge without increased risk of infection to the staff. A significant proportion of patients with respiratory failure presents with relevant hypoxemia, often also caused by a high inspiratory oxygen fraction (FiO2) including NHF, and this hypoxemia cannot be not completely corrected. In this situation, CPAP/NIV therapy can be administered under use of a mouth and nose mask or a respiratory helmet as therapy escalation, as long as the criteria for endotracheal intubation are not fulfilled.In acute hypoxemic respiratory insufficiency, NIV should be performed in an intensive care unit or in a comparable unit by personnel with appropriate expertise. Under CPAP/NIV, a patient can deteriorate rapidly. For this reason, continuous monitoring with readiness to carry out intubation must be ensured at all times. If CPAP/NIV leads to further progression of ARI, intubation and subsequent invasive ventilation should be carried out without delay if no DNI order is in place.In the case of patients in whom invasive ventilation, after exhausting all guideline-based measures, is not sufficient, extracorporeal membrane oxygenation procedure (ECMO) should be considered to ensure sufficient oxygen supply and to remove CO2.