Medscape

Sharon Worcester

Gerry Gajadharsingh writes:

 “A worrying dilemma for doctors deciding if and when to put a COVID 19 patient with pneumonia on mechanical ventilation at the moment is that about 50% sadly die.

 Whilst this may be because of the nature of the virus, doctors and scientists around the world are beginning to question why, and more importantly, are they able do anything to help more people survive.

 The article below came out yesterday and it just arrived in my inbox from Medscape.

What I find fascinating is that the 2 doctors concerned, one from the USA and one from Germany, are proposing that the protocol many medics are following for mechanical ventilation of COVID 19 patients may not be the best for many patients. Many doctors are following a protocol developed for Acute Respiratory Distress Syndrome (ARDS) and the suggestion is that for a fair proportion of those patients that protocol may not be helpful.

 “This is a kind of disease in which you don’t have to follow the protocol – you have to follow the physiology,” he said. “Unfortunately, many, many doctors around the world cannot think outside the protocol.”

 Please note the article is clinically complex but the jist is that they are proposing 5 different treatment models for mechanical ventilation for COVID 19 patients who are seriously affected thus needing mechanical ventilation.

 One of the things that I struggle with in conventional medicine is following protocols. Patients are individuals and to me it makes sense to follow the physiology of a patient, or rather their altered physiology and function, in deciding what type of treatment they need.

 I think about the numerous patients that I have seen over the years where they have been told by other clinicians that they cannot find obvious pathology, i.e. an actual disease process, and therefore there is no underlying medical diagnosis. And yet there must be a cause of their problems.

 There are also many patients who also say I feel fine therefore I must be. I can absolutely tell you this is sometimes not the case. The many homeostatic processes of the body are constantly working to minimise obvious symptoms. It is often the breakdown of these homeostatic mechanisms that lead to actual disease processes, or to an immune system that can’t deal with a pathogen such as a virus.

 Why are 80% of the population predicted to get no symptoms, mild or moderate symptoms even though exposed to COVID 19? It must be something to do with the robustness of their physiology and their immune systems.

 I have written previous blogs on the things people can do to support their own immune systems.

https://www.thehealthequation.co.uk/the-health-equation-blog/

 I wonder whether at least some of the patients who are sadly dying of COVID 19 and reported to have had no underlying medical problems prior to succumbing to the virus, actually fall into the category of disturbed physiology. Obviously knowing this is sadly no use to those patients now. But it may help others realise and better understand what they can do the help support their own physiology and immune systems.

 One of the problems of course is capacity and medical systems around the world are overwhelmed. Medical staff are doing their best to save as many as they can. The situation is evolving so quickly it is difficult to keep up and medics are having to learn as they go. Not ideal but the reality of pandemics.”

 

Physicians in the COVID-19 trenches are beginning to question whether standard respiratory therapy protocols for Acute Respiratory Distress Syndrome (ARDS) are the best approach for treating patients with COVID-19 pneumonia.

At issue is the standard use of ventilators for a virus whose presentation has not followed the standard for ARDS, but is looking more like high altitude pulmonary (o)edema (HAPE) in some patients.

In a letter to the editor published in the American Journal of Respiratory and Critical Care Medicine on March 30, and in an editorial accepted for publication in Intensive Care Medicine, Luciano Gattinoni, MD, of the Medical University of Göttingen in Germany, and his colleagues make the case that protocol-driven ventilator use for patients with COVID-19 could be doing more harm than good.

Dr. Gattinoni noted that COVID-19 patients in intensive care units in northern Italy had an atypical ARDS presentation with severe hypoxemia and well-preserved lung gas volume. He and his colleagues suggested that instead of high positive end-expiratory pressure (PEEP), physicians should consider the lowest possible PEEP and gentle ventilation-practicing patience to “buy time with minimum additional damage.”

Similar observations were made by Cameron Kyle-Sidell, MD, a critical care physician working in New York City, who has been speaking out about this issue on Twitter and who shared his own experiences in a video interview with WebMD chief medical officer John Whyte, MD.

The bottom line, as Dr. Kyle-Sidell and Dr. Gattinoni agree, is that protocol-driven ventilator use may be causing lung injury in COVID-19 patients.

Consider Disease Phenotype

In the editorial, Dr. Gattinoni and his colleagues explained further that ventilator settings should be based on physiological findings — with different respiratory treatment based on disease phenotype rather than using standard protocols.

“This, of course, is a conceptual model, but based on the observations we have this far, I don’t know of any model which is better,” he said in an interview.

Anecdotal evidence is increasingly demonstrating that this proposed physiological approach is associated with much lower mortality rates among COVID-19 patients, he said.

While not willing to name the hospitals at this time, he said that one center in Europe has had a 0% mortality rate among COVID-19 patients in the intensive care unit when using this approach, compared with a 60% mortality rate at a nearby hospital using a protocol-driven approach.

In his editorial, Dr. Gattinoni disputed the recently published recommendation from the Surviving Sepsis Campaign that “mechanically ventilated patients with COVID-19 should be managed similarly to other patients with acute respiratory failure in the ICU.”

“Yet, COVID-19 pneumonia, despite falling in most of the circumstances under the Berlin definition of ARDS, is a specific disease, whose distinctive features are severe hypoxemia often associated with near normal respiratory system compliance,”

Dr. Gattinoni and colleagues wrote, noting that this was true for more than half of the 150 patients he and his colleagues had assessed, and that several other colleagues in Northern Italy reported similar findings. “This remarkable combination is almost never seen in severe ARDS.”

Dr. Gattinoni and his colleagues hypothesized that COVID-19 patterns at patient presentation depend on interaction between three sets of factors: 1) disease severity, host response, physiological reserve and comorbidities; 2) ventilatory responsiveness of the patient to hypoxemia; and 3) time elapsed between disease onset and hospitalization.

They identified two primary phenotypes based on the interaction of these factors: Type L, characterized by low elastance, low ventilator perfusion ratio, low lung weight, and low recruitability; and Type H, characterized by high elastance, high right-to-left shunt, high lung weight, and high recruitability.

“Given this conceptual model, it follows that the respiratory treatment offered to Type L and Type H patients must be different,” Dr. Gattinoni said.

Patients may transition between phenotypes as their disease evolves. “If you start with the wrong protocol, at the end they become similar,” he said.

Rather, it is important to identify the phenotype at presentation to understand the pathophysiology and treat accordingly, he advised.

The phenotypes are best identified by computed tomography scan, but signs implicit in each of the phenotypes, including respiratory system elastance and recruitability, can be used as surrogates if CT is unavailable, he noted.

“This is a kind of disease in which you don’t have to follow the protocol – you have to follow the physiology,” he said. “Unfortunately, many, many doctors around the world cannot think outside the protocol.”

In his interview with Dr. Whyte, Dr. Kyle-Sidell stressed that doctors must begin to consider other approaches. “We are desperate now, in the sense that everything we are doing does not seem to be working,” Dr. Kyle-Sidell said, noting that the first step toward improving outcomes is admitting that “this is something new.”

“I think it all starts from there, and I think we have the kind of scientific technology and the human capital in this country to solve this or at least have a very good shot at it,” he said.

Proposed Treatment Model

Dr. Gattinoni and his colleagues offered a proposed treatment model based on their conceptualization:

  1. Reverse hypoxemia through an increase in FiO2 to a level at which the Type L patient responds well, particularly for Type L patients who are not experiencing dyspnea.
  2. In Type L patients with dyspnea, try noninvasive options such as high-flow nasal cannula, continuous positive airway pressure, or non invasive ventilation, and be sure to measure inspiratory esophageal pressure using osophygeal mamometry or surrogate measures. In intubated patients, determine P0.1 and P occlusion. High PEEP may decrease pleural pressure swings “and stop the vicious cycle that exacerbates lung injury,” but may be associated with high failure rates and delayed intubation.
  3. Intubate as soon as possible for esophageal pressure swings that increase from 5-10 cmH2O to above 15 cmH2O, which marks a transition from Type L to Type H phenotype and represents the level at which lung injury risk increases.
  4. For intubated and deeply sedated Type L patients who are hypercapnic, ventilate with volumes greater than 6 mL/kg up to 8-9 mL/kg as this high compliance results in tolerable strain without risk of ventilator-associated lung injury. Prone positioning should be used only as a rescue maneuver. Reduce PEEP to 8-10 cmH2O, given that the recruitability is low and the risk of hemodynamic failure increases at higher levels. Early intubation may avert the transition to Type H phenotype.
  5. Treat Type H phenotype like severe ARDS, including with higher PEEP if compatible with hemodynamics, and with prone positioning and extracorporeal support.

Dr. Gattinoni reports having no financial disclosures.