This report reveals a mortality rate of 9 % among the first 22 patients to receive active treatment for COVID-19 in the intensive care department at Oslo University Hospital, Ullevål. Half of the patients were not intubated or given mechanical ventilation, even though they had severe hypoxaemia and symptoms of acute respiratory failure according to the Berlin criteria (3). These patients all seem to have had good outcomes, with relatively short stays in the intensive care department. A strikingly high proportion of the patients in intensive care were overweight.
Gattinoni et al. discuss whether mechanical ventilation with a traditional approach to acute respiratory distress syndrome may in some cases do more harm than good for COVID-19 patients. They recommend a more personalised approach based on patient phenotype, and have therefore divided patients into two groups: phenotype L with little lung stiffness and almost normal compliance, and phenotype H with increasing oedema, reduced aerated lung volume and significant lung stiffness with low compliance (11, 12). In type L patients, severe hypoxaemia is the result of both hypoxic vasoconstriction and failure of perfusion autoregulation. The proportion of collapsed lung tissue is low and there is limited potential for recruitment. The use of mechanical ventilation with overly high PEEP therefore seems unnecessary for these patients (11, 12). Initial interventions for these patients may include increasing the oxygen supply via various mask-based systems or non-invasive ventilation, although this is controversial (2), (4–6).
The patients in our ward cohorts received up to 10–15 litres of oxygen by mask with careful monitoring of NEWS, which was scored several times per nursing shift (8), along with measurement of arterial blood gases when indicated. In addition to daily meetings, clinicians on the wards contacted their counterparts in intensive care when needed, and any patients who showed increasing respiratory distress/signs of exhaustion were transferred to intensive care. Nevertheless, several of the patients were able to manage with only supplementary oxygen delivered via various mask-based systems. We found that despite clinically and radiologically severe respiratory failure, it was possible to use intermittent non-invasive ventilation successfully and thereby avoid intubation in some motivated patients (2), (4–6).
It is important to emphasise the need for the continuous presence of experienced intensive care nurses around all intensive care patients, especially hypoxaemic patients who are breathing independently with the aid of an oxygen mask or non-invasive ventilation. Active mobilisation with frequent changes in position, physiotherapy and personalised pain management/sedation are other key components of this intensive care treatment. It must also be stressed that a patient who is breathing spontaneously but with high respiratory effort and pronounced use of the respiratory muscles may generate a significant negative pressure in the pleural cavity, with an ensuing high transpulmonary pressure. A high transpulmonary pressure increases strain on the lungs and risks exacerbating the patient's respiratory failure (patient self-inflicted lung injury, P-SILI) (12, 13). Patients must therefore be closely monitored with respect to the need for intubation.
In line with international experience, in the early stages of mechanical ventilation therapy we used low tidal volume, low plateau pressure, low driving pressure, occasionally high PEEP (up to 14–16 cm H2O) and frequent prone positioning (2, 5, 8)(8–10). This was despite the fact that the lungs of most patients had almost normal compliance (> 50 ml/cm H2O). We eventually found that PEEP could often be reduced to 8–10 cm H2O without compromising oxygenation or compliance. However, some patients required increasing or sustained high PEEP and repeated prone positioning to maintain an adequate level of oxygenation. It is thus conceivable that in some patients we observed a progression from phenotype L to H (11–13). These patients had extensive pulmonary changes on CT, a large proportion of non-ventilated lung tissue and thus a greater potential to benefit from higher PEEP and prone positioning.
The theories of Gattinoni et al. are based on experience with COVID-19 as well as previous research on acute respiratory distress (syndrome) (7), (11–13). In any case, their description of the two phenotypes is consistent with our observations. We therefore believe that in many cases, even with significant hypoxaemia, intubation can be delayed if supplementary oxygen alone, non-invasive ventilation or nasal high flow produce satisfactory clinical improvement and the patient is not exhausted. However, the need for intubation must be continuously assessed, and any mechanical ventilation that follows intubation should be tailored to the patient's pulmonary physiology and clinical condition.
This requires round-the-clock care by experienced intensive care personnel with an understanding of pulmonary physiology and of advanced, careful mechanical ventilation, and who can closely monitor compliance, tidal volume, plateau pressure and titration of PEEP. All of this combined may potentially reduce the risk of phenotype L developing into phenotype H and life-threatening hypoxaemia (11–13). However, distinguishing between these two phenotypes in an individual patient is not necessarily straightforward, and there will be a degree of overlap. CT scans may be helpful, and we recommend systematic measurement of static compliance in all patients receiving mechanical ventilation.
It is important to recognise that the extent of this disease and the pandemic means that treatment must be viewed as a dynamic process in which we are open to changing course and strategy based on our own and others' experiences and knowledge.