Questions related to ARDS
Stellate ganglion block with neural therapy preventing sympathetic nerve system hyperactivity in Covid-19 patients and hypothetically preventing severe ARDS?
Do we have any specific methodology or criteria on how to calculate the utility measures in patients with a worsened outcome in ARDS?
I mean, can we consider their utility score as zero, or something else, while we compare their QoL with those who are survived or died (already zero)?
Do we have any such kind of study for reference? I could find many studies among those who are survived.
Your efforts are much appreciated.
ICU patients who are receiving invasive mechanical ventilation and noninvasive ventilation often require sedation and analgesia. COVID-19 pneumonia / ARDS induced acute respiratory failure patients are not indifferent in this aspect. Sometimes, it also feels that these patients need more sedation, even on NIV. I shall be delighted to know the sedation practices, drugs, single or combinations you are using in your set-up.
New theory is coming up for lung involvement in COVID 19. Based on observations in USA, Spain, Italy.
Most of the postmortem revealed pulmonary thorombosis not typical ARDS...... also patient hypoxemia not responding to PEEP but high Fio2 .
Like methemoglobin, the virus structural protein, sticks to heme - displaces oxygen - displaces iron - free iron toxicity causes inflammation of alveolar macrophages- leads to CT scan changes. No benefit of invasive ventilation . May require frequent blood transfusions.
The virus attacks beta chain, dissociates heme, removing iron & converting it to porphyrin.
Virus can dissociate oxy-Hb, carboxy-Hb and glycocilated Hb.
Lung inflammation from inability of both oxygen & CO2 exchange & ground glass x rays, like CO2 poisoning.
Chloroquine competes the binding to porphyrin.
Favipiravir binds to the virus envelope protein with very high affinity, prevents entry into the cells as well as binding of structural protein to porphyrin.
I have received above mentioned theoretical matter on internet.....
More and more research work is to be done to confirm it.....
Dear critical care enthusiasts
Is there any epidemiological study conducted in India showing incidence and pattern of ARDS in a large population? Any multicentric study?
I could not find the exact incidence of ARDS in India anywhere during the literature search. Please help.
Thank you. Regards Dr Mohd Saif Khan, MD, DNB, Postdoctoral fellowship in critical care (JIPMER), DM critical care medicine (TMH Mumbai), MNAMS Associate Professor Dept. of Critical Care Medicine Trauma Centre and Central Emergency Rajendra Institute of Medical Sciences Ranchi-834009, Jharkhand, India
One of the problem for managing COVID19 patients is excess respiratory drive. So we use Neuromuscular blockade to prevent P-SILI and VILI. In some cases, we have to use these drugs for greater than 48 hour. Is it Safe or Not ? What do you think? and How do you manage these patients in your unit?
June 16, 2020: Publication today from Oxford alleges that oral dexamethasone is a "cure" for COVID-19.This was also just announced on the National News broadcasts. This is after much work using high dose steroids as per usual in severe pneumonia with ARDS, etc. which didn't seem to work in COVID-19. Even severe asthma is treated with large doses of steroids, so at this point at least, I do not really understand their claim. I will continue to study this and let you know. If anyone else has more insight, please let us know.
Could ARDS in Covid-19 patients result from inferior waste clearance by a compromised lung microvasculature causing local build up of excess cytokines?
I am VERY unimpressed with the magnitude of elevation of cytokine levels via blood tests. If I correctly recall some analyses I conducted on patterns of cytokine elevations during cytokine storms, you would see many multiple units of magnitude deviation from normal values. Covid-19 patient values are far from this, and it seems like labeling these blood levels as storms is a stretch. Thoughts? Am I mistaken?
Further, death attributable to organ damage associated with uncontrolled cytokine storms kill the young with robust immune systems. These storms are generally considered an over-reaction of a healthy immune system. Covid-19 is remarkably sparing of the young. Covid-19 is burning through the old and elderly, particularly men. These guys can barely get a good piss going, no less any kind of big storm.
Interestingly, I DO believe that a sizable contribution to patients developing ARDS is due to extensive damage to lung tissue attributable to a cytokine response. I believe there is a localized cytokine storm in lungs attributable to lack of normal, timely clearance. Creation of tissue damage due to slow clearance, this new lung tissue damage provokes a second cytokine response.....
Reviewing list of comorbidities significantly associated with Covid-19 patient death, with the exception of heart disease, I believe they all share a major common, physiological impact. Diabetes, high blood pressure, ......regularly lead to narrowing of capillaries as well as loss of their flexibility to expand is well documented as present lung tissue, among many places. This may impact effective clearance of over-sized WBCs as body is actively battling an infection, further degrading waste clearance ability by slowing or blocking blood flow.
As for obesity, it is highly coincident with high blood pressure and diabetes, so I suspect it’s association with increased mortality is predominantly mediated through the effects of the other significant comorbidities.
Heart disease is the exception that proves the rule. Great stress is placed on the heart under the unrelenting pressure to increase throughput in response to oxygen starved systems, even while it is also oxygen starved. This is not a sustainable situation in any event, and has an even shorter time horizon with an unhealthy heart.
Ive read that many believe the deficiency in ACE2 by Coronavirus interferes with normal vasculature regulation and that has prompted trials of ACE inhibitors to further drive regulation through a sole mechanism prompting a increased blood flow. Could work if vasculature can be responsive, can’t work if microvasculature is to compromised by effects of comorbid conditions.
Has this already been discussed by others elsewhere?
It has already applied the principles of 'permissive hypercapnia' during mechanical ventilation in several clinics at ARDS of COVID-19 patients, which is likely to save lives. Nevertheless, treating ARDS with mechanical ventilation is not a 21st-century solution. I had stated that hypocapnia could cause vicious circles and death at critically ill patients. Several vicious circles have also been identified in ARDS, and hypocapnia may also play a role in them, for example, enhances pulmonary hypertension and decreases surfactant formation. Does the question arise, whether the vicious circles can be stopped even before ARDS develops? Surprisingly few works of literature are known to use a mixture of carbon dioxide and oxygen therapeutically at any disorders. Administration of 5% carboxygene in animal experiments reversed the process of surfactant depletion.
Immune responses to infections with by a corona virus vary widely and are appear to be related to the development of most severe complication, acute respiratory distress syndrome. Since survival of patients respondingto the virus in this way depends on respirators support, mechanical ventilation and extracorporeal oxygenation, therapeutic methods which demand highly specialized medical and nursing staff, human resources which become scarce in an epidemic or pandemic. Since vaccination are not available in newly emerging corona virus epidemics it would be interesting to know if and which targeted pharmacological modulation of immune response early in the course of an infection could help to reduce the need for intensive care and/or improve the outcome of respiratory support.
Differences in immune responses to emerging corona viruses and the difficulties of developping vaccines contribute to a surge in ARDS in vulnerable populations, leading to acute shortages and disruptions in health care logistics and delivery, notabily in technical and human resources for intensive care (mechanical ventilation and extracorporeal oxygenation). It would therefore interesting to know which pharmacological interventions in early stages of corona virus infections could modulate the immune response in a way to reduce the number of cases with progression to ARDS or mitigate the respiratory complications related to COVID-19, in order to maintain functioning of the health care system and to avoid irrational allocations of resources (e.g.purchasing hundreds of ventilators by institutions which are unable to provide the medical and nursing staff needed to use them). Does anybody know of recent observations that hint at a role of pharmacological interventions which could contribute to improved outcomes?
Gralinski LE, Sheahan TP, Morrison TE, et al. Complement Activation Contributes to Severe Acute Respiratory Syndrome Coronavirus Pathogenesis. mBio. 2018;9(5):e01753-18. Published 2018 Oct 9. doi:10.1128/mBio.01753-18
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Covid-19 cases, who are developing severe ARDS / respiratory failure are requiring mechanical ventilation, and the number of such cases is increasing during this pandemic. However, even in the countries having advanced and robust health care facilities are failing to provide an adequate number of ICU beds and Ventilators for such increasing numbers of patients. Healthcare providers of many areas are now using one ventilator for providing mechanical ventilation to multiple patients simultaneously. As most of the ventilators can not provide differential ventilation (even those which can, are designed for two lungs at most 2 patients), is it safe to do so? As the compliance of the lungs of the different patients will be different, their PS, Vt and MV required will be different, how it can be feasible? Isn't there a chance of cross-infection / super-infection? Please opine and guide..
I am researching the function of neutrophil elastase in lung diseases such as the ARDS. But I cannot find any information or papers to look into the expression of mRNA level of the neutrophil elastase from the bone marrow derived neutrophil. If you have done the tests, can you let me know what and how much stimulator would be used for the nutrophil to express the mRNA of neutrophil elastase?
Sorry for the tangent. The article was interesting. MRSA IS A SERIOUS PROBLEM, I wonder if the answer is not going to involve thinking outside the box. I was reading an article on this site about a plant in Iran I think. It retards or kills MRSA. What if bandages could be impregnated with this, or bedding to control the spread of this terrible disease or even cleaning products?
Please take part to this international survey (3 minutes!). We want to know how you manage anticoagulation, including antithrombin supplementation, during veno-venous ECMO. Your contribution will be acknowledged in case of publication (this is why the survey is not anonymous).
I am looking for the paper, "Neuropsychological sequelae in survivors of ARDS compared with critically ill control patients". I requested it 21 days about, but I am still waiting to receive the article. If anyone has a copy of the article, I would like a copy. Thank you.
Controlling the tidal volumes and the distending pressures when ventilating patients with ARDS is the standard of care. An important publication also showed that the use of paralysis early in the course of disease decreased mortality. That is likely related to better ventilation control and decrease of 'double triggering', which adds two breaths to generate one large breath. However, spontaneous respiratory efforts have benefits. As patients get better they are usually transitioned to assisted spontaneous breathing. How do you decide when to make that transition?
We are currently heading towards the completion of a pilot trial. Interested in knowing experience and perceptions of other pediatric intensivists around the world.
There are many markers of endothelial activation and damage (sVCAM-1, von Wilebrand factor, D-dimer, etc. etc. etc.), and I need to decide for one (ideally) or two to measure in human blood that can tell me if the endothlium has been activated, damaged or dead. We want to look for indicators of activation of any vascularity that can have impact at a systemic level, to the point of possibly participating in septic shock or acute respiratory inflammatory syndrome, empyema, lung edema, deep vein thrombosis, etc (any poor outcome related with inflammation). The patiens will be mainly critical or hospital-bound, with respiratory symptoms, mainly related with infectious diseases. I will thank any ideas.
I've been doing some experiments using intranasal dosing of LPS, a technique that has been well described in the literature and I achieve very uniform results (on the whole). Occasionally there will be a mouse that I believe hasn't had the dose as their lungs show very little sign of injury, and no sign of systemic illness. I am loath to discard the results from these mice as it could be that these animals are protected for a specific reason, or it could mean that the dose was swallowed during dosing. Does anyone know of a measurement that could be taken after dosing to ensure that the LPS did reach the lungs? That way I could confidently exclude the tiny minority of mice that I believe didn't receive the full dose.
All the best,
I think everything is almost in the title of topic. I'd like to know how is it possible to know if my amino acid sequence contains ankyrin repeats? I know predicting programs for coiled coil domain for example but not ARD.
Thanks in advance for your help
Have a nice day
Big trials came with no mortality benefits from HFOV in ARDS cases, although bed side management for these patients with HFOV, showed some benefits?
In some instances, the underlying cause of acute respiratory failure can not be identified using laboratory, radiological and minimally invasive diagnostic procedures (including bronchoscopic BAL). Do you at all consider surgical lung biopsy a useful option in this situation? And if so, what is your trigger to request a biopsy? What are your contraindications?
Our paper recently published in the J Trauma demonstrated that application of Airway Pressure Release Ventilation (APRV) after injury (i.e. fecal peritonitis and gut ischemia/re-perfusion) prevented lung injury in a porcine ARDS model. We hypothesize that this strategy will also work in humans at risk of developing ARDS so my question to the ICU clinicians is has anyone used a preemptive ventilation strategy to prevent rather than treat ARDS in humans?
What are the common methods for recruitment? Are sigh, SI and e-sigh very commonly used?
Were you surprised by the two studies published in the NEJM, Oscar and Oscillate? Is the benefit of HFOV lost in the era of low volume, pressure limited ventilation for ARDS? Will you continue using HFOV for rescue therapy or jump to extracorporeal support instead? Why do you think Oscillate had a higher mortality in the HFOV group?
The number of patients under mechanical ventilation increases, but we have limited health professionals in our ICU so, it would be better to have the automated MV, to protect the patients.