key: cord-310069-ay4af6xr authors: Tobin, Martin J. title: Does making a diagnosis of ARDS in COVID-19 patients matter? date: 2020-07-21 journal: Chest DOI: 10.1016/j.chest.2020.07.028 sha: doc_id: 310069 cord_uid: ay4af6xr nan The question "Do patients with COVID-19 develop typical ARDS?" is arousing fevered debate. Respondents pivot their answers around the nature of COVID-19, rather than ARDS. The controversy unveils riddles at the core of ARDS. What exactly is ARDS, and how should a doctor decide whether some patient has ARDS or another disorder? In the founding report, Ashbaugh and Petty christened the new disorder a "syndrome" because it encompassed a grouping of clinical and pathophysiologic abnormalities with no known cause. 1 After its baptism, its very existence was called into question. Dr. Fishman, editor of the first multivolume textbook of pulmonary medicine, denigrated it a "distinctive non-entity." Another critic remonstrated that making a diagnosis of "ARDS is not helpful because it obscures a clinically very important differential diagnosis". 2 That grumbler was Dr. Murray, who later enumerated a scoring system to adjudge whether or not a patient has ARDS. Dr. Murray never explained his volte-face in resurrecting a syndrome he had previously tried to terminate (RIP). 2 Subsequent panels-American-European Consensus Committee (AECC) and Berlin panelrearticulated criteria for defining ARDS. Designated criteria were chosen with a goal of setting tight boundaries to achieve greater uniformity of patients being enrolled in clinical trials. Each new formulation was justified by specifying grave flaws in its predecessor. None of the redefinitions represented a radical change from Ashbaugh and Petty's initial description. The Berlin definition claims that ARDS can be diagnosed only if onset is within 7 days of a known insult. Observing that respiratory failure occurred 8-12 days after first symptoms of 3 COVID-19 in Chinese series, Li and Ma 3 concluded that these patients should not be diagnosed as ARDS. Other commentators consider high compliance measurements as grounds for doubting typical ARDS in COVID-19 patients. The claims and counterclaims fail to acknowledge that ARDS is a man-made creation. Contrast ARDS with measles, which is caused by a non-redundant etiologic agent (virus), with uniform pathogenesis and a rash so characteristic that diagnosis is self-evident. Nosologically, measles constitutes a "natural kind" on etiologic, pathogenetic, and clinical levels. ARDS does not represent a natural kind on any level. Each constituent in ARDS definitions has fuzzy boundaries. Hypoxemia is identified by In ARDS patients with fixed shunt, alterations in F I O 2 caused PaO 2 /F I O 2 to fluctuate unpredictably by more than 100 mmHg. 4 In patients fulfilling all ARDS criteria, administration of 100% oxygen for 30 minutes caused PaO 2 /F I O 2 to increase such that 58.5% were no longer categorized as ARDS. 5 When ARDS-Network researchers interpreted chest x-rays according to AECC criteria, agreement was only moderate (kappa=0.55) with full agreement on less than half the radiographs. 6 This poor performance was one justification for developing the Berlin definition. Subsequent evaluation of the Berlin criteria found interobserver agreement no better (kappa=0.50), with 67% disagreeing on imaging interpretation. 7 4 Too much attention is focused on the definition of ARDS. Placing it on an altar for veneration is unwarranted. Getting pedantic as to whether a COVID-19 patient truly satisfies criteria for ARDS is a distraction from patient care. Definitions beget a sense of finality (often unjustified), and can confine the mind rather than liberate it. Few diagnoses dictate an invariant course of action. Diagnosing pneumothorax is not inevitably followed by needle drainage-high concentration of oxygen is preferable in certain circumstances. All patients with ARDS do not require intubation; some are sustained with supplemental oxygen or noninvasive ventilation. A central criticism of ARDS is its heterogeneity; diagnosing ARDS may halt the search for the underlying cause. 8 This criticism does not apply to respiratory failure in COVID-19 patients: we know it is caused by SARS-CoV-2 and no therapy is effective against the virus. The only consequent of ARDS diagnosis is avoiding tidal volume 12 ml/kg. Given that tidal volume 12 ml/kg is not employed in any patient, making a diagnosis of ARDS does not impact selection of any ventilator setting. Tidal volume 6 ml/kg has not been proven superior to tidal volume 11 ml/kg (or anything in between)-nor is 6 ml/kg appropriate in every patient. Decrements in tidal volume are necessarily accompanied by shortening of mechanical inspiratory time. Once mechanical inspiratory time becomes less than the patient's neural inspiratory time, double triggering is inevitable. 9 A doctor may set tidal volume 6 ml/kg, but the patient is receiving 12 ml/kg. Identifying phenotypes and endotypes arouses much interest-but this is still (sub)group thinking. Searching for subgroups is apposite for research investigations but not applicable for individualized care. The mindset for care at the bedside is antithetical to that needed for conducting clinical trials. Each patient is unique-even twins from the same ovum are different. Respiratory physiology in ventilated patients is complex. It is impossible to predict the net response of multiple counterbalancing reflex pathways incited by a single alteration in a ventilator setting. There is no substitute for making changes and observing the effect on plateau pressure, airway pressure waveform, double triggering, PaO 2 , blood pressure and so on. 9 And then iteratively fine-tuning the settings. Based on personal experience of teaching residents at the bedside for more than four decades, the cognitive task trainees find most challenging is to separate wheat from chaff-to ward off distractions in a complex case and identify the pivotal factor that will decide a patient's outcome. For the doctor at the bedside of a COVID-19 patient, making a diagnosis of ARDS is completely irrelevant. No clinical action will follow directly from the diagnosis. The debate presently raging 6 as to whether COVID-19 produces typical or atypical ARDS is an unfortunate distraction from the central questions that decide a patient's outcome. The cognitive challenges in COVID-19 revolve around interpretation of blood oxygen levels 10, 11 and deciding whether to insert an endotracheal tube. 12 It is a tragedy to think that some COVID-19 patients were intubated simply because oxygen was being delivered at more than 6 liters/min targeted to a non-scientific pulse oximetry objective. We tend to forget that diseases have no separate existence independent of patients. As doctors we treat patients, not diseases. Management requires customized care, tailored to each patient's unique physiological response-not mindlessly following a protocol assembled for an ARDS cookbook. Acute respiratory distress in adults Editorial: The adult respiratory distress syndrome (may it rest in peace) Acute respiratory failure in COVID-19: is it "typical Variability of indices of hypoxemia in adult respiratory distress syndrome Screening of ARDS patients using standardized ventilator settings: influence on enrollment in a clinical trial Interobserver variability in applying a radiographic definition for ARDS Interobserver Reliability of the Berlin ARDS Definition and Strategies to Improve the Reliability of ARDS Do we need ARDS? Principles and Practice of Mechanical Ventilation Basing respiratory management of COVID-19 on physiological principles Why COVID-19 silent hypoxemia is baffling to physicians Caution about early intubation and mechanical ventilation in COVID-19 Abbreviations List: AECC: American-European Consensus Committee ARDS: Acute respiratory distress syndrome COVID-19: Coronavirus disease Fraction of inspired oxygen PaO 2 : Partial pressure of oxygen in arterial blood PEEP: Positive end-expiratory pressure SARS-CoV-2: Severe acute respiratory syndrome coronavirus 2