Between the discovery of a virus and the development of a vaccine, it usually takes several years. But the health emergency can speed up the process.
Eighteen months: this is the time evaluated and hoped for by the researchers for the development of a vaccine against the new coronavirus. This period may seem long for a confined population, prohibited from leaving for lack of treatment. However, the health emergency of the situation has meant that this period has been greatly shortened: normally, it generally takes around ten years to create a vaccine.
Why so long? How do researchers work? Why can we go faster today? Why is a vaccine needed to stop the pandemic?
The treatment of Covid-19 patients with respiratory failure due to pneumonia is based on respiratory assistance in approximately 5% of cases. In severe forms of the disease, respiratory involvement can indeed lead to acute respiratory distress syndrome (ARDS), a pathology which is responsible for 30%, even 50%, mortality in patients on artificial respirators (invasive ventilation).
It quickly became apparent that the acute respiratory distress syndrome associated with Covid-19 does not resemble the majority of conventional ARDS. While in half the ARDS cases the lung loses some of its elastic properties, the lung remains distensible at the initial stage of Covid-19 pneumonia.
It retains its ability to normally vary its volume as a function of the variation in intrapulmonary pressure. Specialists speak of preserved “compliance”. In other words, the lung retains its elasticity. Consequence: the lung remains ventilated: the amount of intrapulmonary air is normal or close to normal.
In fact, Covid-19 pneumonia can present clinically in a very heterogeneous way. For the same degree of hypoxemia, some Covid-19 patients have more or less significant difficulty in breathing, a more or less rapid respiratory rate. Thus, Covid-19 patients with very low levels of blood oxygenation (deep hypoxemia) may experience very different symptoms.
Some may have normal breathing. Their hypoxemia is said to be “silent”, while others have pronounced difficulty in breathing. Likewise, some patients are improved by lying down, others are not. Some respond positively to the inhalation of nitric oxide, a gas that causes vessels to dilate, others do not. Finally, some patients have a significant decrease in the amount of carbon dioxide (CO2) in the arterial blood, while others have a normal or abnormally high level of carbon dioxide.
The diagnosis of an ARDS is conventionally based on well-defined parameters. Resuscitation doctors speak of the “Berlin criteria”, the city in which experts met in 2012 under the aegis of the European Society of Intensive Care Medicine (ESICM) to define the clinical, ventilatory, gasometric parameters (analysis of blood gas) and radiological tests to establish the diagnosis of this serious pulmonary syndrome and to best adapt the ventilatory management.
To this characteristic, not usually observed in most ARDS, is added another parameter, clinical this time, in relation to what specialists call hypoxemia, a term used to designate the decrease in the amount of oxygen in the blood. Many Covid-19 patients with pneumonia have been found to be surprisingly tolerant of the low level of oxygenation of the blood associated with pulmonary involvement. This extreme tolerance to hypoxia in many patients is a real peculiarity of Covid-19 pneumonia.
Many Covid-19 patients, however very hypoxemic, express themselves normally, calmly watch television or play on their smartphone, without experiencing any particular difficulty in breathing or without having a high respiratory rate. However, given their low level of oxygen in the blood, doctors would expect them to go wrong, in other words that they present clinical signs suggestive of acute respiratory distress syndrome (ARDS). It shows that you shouldn’t just base your attitude on blood gas results. It is ultimately the clinical condition of the patient that counts.
It is likely that this diversity of pulmonary clinical presentation in Covid-19 patients hospitalized in emergency is due to the interaction of many factors: the severity of the viral infection, the immune response, the physiological reserve (in other words the capacities of adaptation to the effort of the patient’s lungs), the presence of pre-existing pathologies (comorbidities), the time between the onset of symptoms and admission to hospital.
All the clinical, radiological and histological data accumulated over the past few weeks show that the understanding of pulmonary involvement linked to Covid-19 is constantly progressing, sometimes thanks to unexpected clinical observations or surprising data.
Understanding the pathophysiological mechanisms underlying the onset and course of this pneumonia is crucial in deciding the most appropriate treatment for each patient in intensive care. In times of health crisis, and perhaps even especially in such circumstances, it is important to produce robust scientific data in order to better understand the pulmonary pathophysiology of Covid19.
And all the more so as it is becoming increasingly clear that in hypoxemiant pneumonia (with low oxygenation in the blood), that associated with SARS-CoV-2 infection is truly unique.