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ARDS - Science topic

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Stellate ganglion block with neural therapy preventing sympathetic nerve system hyperactivity in Covid-19 patients and hypothetically preventing severe ARDS?
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Ganglion block sym supply to cranium not lungs
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Hello Researchers,
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.
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-I-
I do not understand the question: IN SURVIVORS OR "IN NON-SURVIVORS WITH ARDS" ... as and as it literally appears, IT MAKES NO SENSE !!!
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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.
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Dead high: Until I contracted Covid-19 myself, I have been in command of a Covid Care Unit (vaccinating, treating patients with it at all levels and, of course, sedating myself -both to intubate , as in sedation in Palliative Care -PC- including deep and irreversible sedation, if necessary, and with all the legal and bioethical guidelines required).
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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.....
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The relevant question is about coronavirus disease 2019 (COVID-19).
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Yes: Of course!!
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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
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However, the data is from Singapore..not from India. So my question remains unanswered.
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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?
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Many patients who receive prolonged infusions of muscle relaxants develop critical illness polyneuropathy and polymyopathy.
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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.
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Dexamethasone - A broad spectrum Livesaving Streoid - Can be used for severe infection but not Covid specific .
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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.
Thoughts?
Has this already been discussed by others elsewhere?
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This paper help you out
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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[2]. I had stated that hypocapnia could cause vicious circles and death at critically ill patients[1]. Several vicious circles have also been identified in ARDS, and hypocapnia may also play a role in them, for example, enhances pulmonary hypertension[3] and decreases surfactant formation[4]. 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.
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Several works of literature demonstrate that hypocapnia (and not metabolic alkalosis!) plays a significant role in the inhibition of surfactant formation.
Today, it also seems to be proven that this is caused by an increase in mitochondrial Ca2+ levels, which means ATP-energy insufficiency.
We do not know how reversible this process is. Ventilator-induced ‘permissive hypercapnia’ already works well, but it’s a little too late for many.
THEREFORE, the lack of surfactant and the development of ARDS should be prevented by raising pCO2 level in anyhow (not with respiratory machinery!). Maybe it's not that hard? At an early stage, perhaps the administration of a small dose of iv. Na-bicarbonate would be sufficient (monitored), taking care not to develop metabolic alkalosis, as well. Therefore, it may still need to be co-administered with carbogen and/or intracellular pCO2-boosting medicine (acetazolamide?).
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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.
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Detection of Immunoglobulin M (IgM), IgA, and IgG Norwalk Virus-Specific Antibodies by Indirect Enzyme-Linked Immunosorbent Assay With Baculovirus-Expressed Norwalk Virus Capsid Antigen in Adult Volunteers Challenged With Norwalk Virus
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Cytokine storm or pulmonary edema the cause of death?
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The median time from SARS-CoV-2 symptom onset to the development of pneumonia is approximately 5 days, and the median time from symptom onset to severe hypoxaemia and ICU admission is approximately 7 - 12 days. The acute hypoxaemic respiratory failure - sometimes with severe hypercapnia - from acute respiratory distress syndrome (ARDS) is the most common complication (in 60-70% of patients admitted to the ICU), while hypoxaemia, without respiratory distress, is developed in few elderly patients. This means that the respiratory problem is the evolution most common that conditions the elevated number of deaths. Data from Intensive Care National Audit and Research Centre (ICNARC), based on a sample of 3883 coronavirus patients, reported that death rate on 2249 patients admitted to intensive care with coronavirus now stands at more than 51% (51.6%), of which 871 patients have died, 818 patients have been discharged alive from critical care and 2194 patients were last reported as still receiving critical care. Of the 871 people who died, 53.6% were male, while 46.3% women. Unfortunately, mechanical ventilation (MV) may amplify the lung-specific inflammatory response in preinjured lungs by elevating cytokine release and augmenting damage to the alveolar integrity, and preinjured lungs are more sensitive to MV at later phases of sepsis, and this situation may be a result of differing immune status. The ventilator-associated lung injury (VALI) are the deleterious effects of high positive pressure ventilation, determined by three mechanisms identified as biotrauma, barotrauma/volutrauma and atelectrauma. In particularly, biotrauma, is the mechanical stimulus that involves the application of positive pressure during mechanical ventilation triggers, through a process of mechanotransduction, a biological response characterized by the secretion of proinflammatory cytokines and the emergence of a neutrophilic infiltrate. As a result, there is a release of inflammatory mediators from the ventilated lung that can lead to a systemic dissemination, contributing to the development of the multiple organ dysfunction syndrome. The biotrauma contributes to the persistence of the inflammatory process and it is associated with worse prognosis in patients with ARDS. In barotrauma/volutrauma, the subjects submitted to high ventilatory pressures showed alveolar damage by over-stretching, consisting in perivascular and alveolar oedema, and that use of high volumes can cause breakage of the alveolar walls. The pulmonary over-stretching is increased due to the coexistence of healthy alveoli and non-aerated collapsed areas. This regional heterogeneity can aggravate the lung damage in previously healthy aerated alveoli and in the interface aerated/non-aerated areas, even when low volumes are used for ventilation. In stelectrauma, the mechanical ventilation may result in cyclic variations of alveoli aeration, that lead to epithelium damage due to the emergence of shear forces at the interfaces between air and fluid in the injured lung, and the generation of open-collapse alveoli phenomena. Therefore, about fifty percentage of patients treated with invasive mechanical ventilation died, and that 53% of deaths were related to respiratory failure.
For to don't be late and avoid, as much as possible mechanical ventilation, is necessary proceed, especially for people ≥60 years, to check, twice day, oxygen saturation and temperature, even if without symptoms and when respiratory rate ≥30 breaths per min, oxygen saturation ≤93%, and temperature ≥37.5 °C, immediately calls service of emergency.
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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?
Lit.
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
Frieman M, Baric R. Mechanisms of severe acute respiratory syndrome pathogenesis and innate immunomodulation. Microbiol Mol Biol Rev. 2008;72(4):672–685. doi:10.1128/MMBR.00015-08
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Early/middle stage:
In the middle stage, where symptoms start occurring, fever activates the innate immune system (whereas Covid-19 suppresses it). Furthermore, fever suppresses immune-overreactions via HSP's & NF-kB regulation. Therefore, fever might help fight off the virus, preventing severe complications.
In this stage of the infection, fever should not be mitigated. Therefore, drugs such as paracetamol, aspirin, NSAID's, or any other COX-2-inhibitor, should not be taken. However, individual circumstances might require these kinds of medication anyway. For instance: Amlodipine could be prescribed as BP-lowering medication. Amlodipine also inhibits COX-2, and therefore mitigates fever. If Amlodipine is prescribed, it should not be stopped. Another example would be someone who takes something like Warfarin. Fever might change INR.
Vitamin D is already mentioned.
severe complication-stage, with Pulmpnary Edema (PE):
- Anti-viral medication (Chloroquine, Remdesivir)
- IL-6-inhibitors (Tocilizumab)
- B2R blockers (Icatibant)
- C5-blockers (Eculizimab)
Anti-viral medication, such as (hydroxy)Chloroquin & Remdesivir, has shown some potential. However, I believe that anti-viral medication could potentially have more beneficial effects earlier on, when complications are not yet present. During severe complications, it is mostly the immune-overreaction that needs to be mitigated. Except from some promising preliminary studies, I do not have any hard data regarding viral inhibitors yet. I believe the side effects of Chloroquine were already mentioned.
Ciclesonide has potentially a double beneficial effects on both inflammation & viral inhibition. I believe a preliminary studie was done in Korea, with promising results. However, to my knowledge there is no hard data yet.
IL-6-mediated endothelial cell contraction increases capillary permeability, causing interstitial PE (imaging: ground-glass opacity), parenchymal infiltration & alveolar collapse (imaging: consolidations). Therefore, inhibiting IL-6 could possibly mitigate these severe complications. Preliminary research shows the effect of Tocilizumab on PE (visible on imaging as decreasing ground-glass opacity). This research is far from perfect, however, and there are serious side effects of IL-6 inhibitors (such as increased risk of secondary infections). There are multiple studies (phase-3-trials) ongoing at the moment, but other than the results from Xu (2020), and anecdotal reports, there is no hard data yet.
Bradykinin (BK), formed by Kallikrein, also increases capillary permeability, and therefore contributes to PE. BK-dependent PE is resistant to corticosteroids (or adrenaline). ACE-2, next to its role in RAAS, also inactivates a BK-variant (that acts mostly on B1R in the lungs). Therefore, Ace-2 mitigates PE. Covid-19 reduces ACE-2, thereby increasing BK, which subsequently increases PE (linking the virus directly to PE). Comorbidities (such as diabetes) also reduce ACE-2, thereby contributing to PE. Blocking the B1R and B2R receptors (or the upstream Kallikrein-process) might mitigate severe complications. Icatibant is a selective B2R-inhibitor (Firazyr). There have been some preliminary good results using Icatibant on covid-19 patients. However, once again, there is no hard data yet (that I know of).
The complement-system activation possibly plays a role in this stage of the disease as well, and C5 blockade (with Eculizimab) might also help (studies are ongoing at the moment).
So, in short, there are a lot of potential mitigating factors, and even though some preliminary studies have been done (with promising results), there is no hard data available (that I know of). I am probably still missing a lot though...
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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..
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Everything in medicine balances risk and potential benefit.
In a crisis situation when I have to intubate a patient but there is no ventilator is available then I would share the ventilator rather than choose which patient should be ventilated.
Is sharing a ventilator less safe than using one ventilator per patient. Not ventilating a patient who needs it will inevitably result in death.
These are difficult times and difficult choices will have to be made.
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Hi!
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?
Thank you!
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I cannot help. I deal only with skin and local pain without AINS treatment
JEAN
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I am a nurse in a CV ICU. We get patients frequently who are positive via nasal culture for MRSA, we also get wounds-sternal incisions, stasis ulcers or arterial compromised wounds with gangrene and MRSA or S.Aureus. I have not seen anyone die from infection directly except a man with such severe endocarditis his mitral valve could not close. He had emergent surgery, we fought to keep him alive. This was 10 years ago, we tried proning him because he went into severe ARDS. Now we would have tried ECCMO maybe, his coags were bad and he had multiple micro clots. He died after two hard weeks.
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?
brigid
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Staphylococcus aureus - A Gm + ve bacteria responsible for infection of sinusties & Upper Respiratory Tract ( URT ) infections . In severe case Pneumonia
may case sepsis leading to death .
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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).
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Dear Alessandro Protti,
VV-ECMO- Veno-Venous ExtraCorporeal Membrane Oxygenation is an artificial Membrane Lung, with its blood pump, placed in series with the failing Natural Lung (NL). The ML can totally or partially take over the functions of the NL in both carbon dioxide removal and oxygen intake. The delivery of O2 to the patient's metabolism and the removal of CO2 depend on a complex interaction between the ML, the NL and the metabolic status. Why anti-thrombin (AT) is needed during VV-ECMO?
-Bleeding is the most feared complication during ECMO and is associated with high dosing of heparin. Although, there is no consensus on antithrombin (AT) supplementation during ECMO, AT is needed by heparin to properly anticoagulate. Heparin is required during ECMO to avoid circuit thrombosis and its anticoagulant effect is strictly dependent on antithrombin (AT). AT also plays a central role in mediating inflammation. Acquired AT deficiency is common in patients on ECMO, arguably due to long term anticoagulation in addition to sepsis itself. AT supplementation increases anti-Factor Xa (anti-Xa) levels without increasing heparin dosage. This may have a clinical impact because risk of bleeding during ECMO is associated with higher heparin dosage. Clinicians strongly believe that maintaining normal antithrombin activity levels (80%-120%) during ECMO will potentially be associated with:
1. Less heparin dosage
2. More adequate level of anticoagulation
3. Less hemostasis related complications, and
4. A lower level of inflammation
See the links below:
Best wishes
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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.
Anita 
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Please find the requested article as a pdf.
Best Chris
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Is there any case reports of ARDS following PGE1 infusion weather in adults after liver transplantation or in peds for PDA?
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Not aware of this being an issue post liver transplantation-
Years ago when we were using it in the setting of poor initial graft function in the liver transplant recipient it was an observation that hypotension could be an issue leading to the PGE1 having to be ceased.
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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?
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Despite the already excellent and thorough  responses to your relevant question I would like to add some comments. 
Transition to spontaneous breathing in ARDS patients is one of the most difficult parts of their ventilatory treatment and the point in time to do so is still under debate. 
It is impossible to set fixed rules but was has been discussed so far are all good advices. It is important to have the precipitating cause of ARDS under good clinical control and to have witnessed an improvement in lung function such as less needs for FiO2, increasing compliance, decreased PEEP needs to maintain the same ventilation targets. It is very difficult to give general threshold values  as this vary from patient to patient. This improvement is generally seen after 2 - 3 days of controlled lung protective mechanical ventilation. 
The transition to spontaneous breathing has to be smooth as the lung is still  very susceptible to suffer from mechanical stress and it is essential to prevent a second hit mechanism at this stage. 
So independently of when it is decided to transit the patient to spontaneous breathing the following must be taken into account: 
Avoid patient-ventilator asynchrony by choosing modes or settings that enhance synchrony. 
Check for increased work of breathing. Prevent the patients from vigorous inspiratory efforts or high respiratory drive as this may cause large transpulmonary pressure changes in different regions of the lung. If this cannot be controlled it might be too soon to transition the patient to spontaneous breathing.   
Controlling tidal volumes is difficult as patients are contributing with their own Pmus Compliance is hard to interpret as the ventilator does not "see" the patient's contribution. In this circumstance a smooth breathing pattern and a low driving pressure may be the best indicators of an appropriate spontaneous breathing. 
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We are currently heading towards the completion of a pilot trial. Interested in knowing experience and perceptions of other pediatric intensivists around the world.
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You can reach me by email. 
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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.
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With regard to sTM, one always has to remember that injured hepatocytes are a very important and abundant source of the circulating molecule (see some of reaserch papers from myself). It limits the use of sTM as an endothelial activation/injury marker, especially in sepsis and multiorgan failure where liver is commonly affected.
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Dear all,
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,
Charly
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A successful administration might change the phenotype of peripheral blood leukocytes. I would try a FACS-staining of PBMC   "before/after" (maybe at different timepoints 2-12h after) and check for expression of CD69 on subpopulations (T cells, B cells, NK cells). In this paper they show that after airway LPS-exposure an increase of CD69 signal can be measured: 
A Ortiz-Stern et al. (2011): Langerin+ dendritic cells are responsible for LPS-induced reactivation of allergen-specific Th2 responses in postasthmatic mice.Mucosal Immunology (2011) 4, 343–353; doi:10.1038/mi.2010.73
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Hi everybody,
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
David
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As far as protein motif and domain family resources such as Pfam, SMART, etc are concerned, the ANK repeat is just another motif/domain. So if you go to InterProScan e.g., a meta-resource that uses and displays the information from about 10 other such resources, or to e.g. Pfam itself, it should detect the ANK repeats if they are present. A good read is also this:
HTH, Rob 
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Big trials came with no mortality benefits from HFOV in ARDS cases, although bed side management for these patients with HFOV, showed some benefits?
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In my Unit, using higher levels of PEEP and recruitment maneuvers in ARDS patients has dramatically decreased  the use of HFO. I strongly believe that previously, we have been inadvertingly recruiting our patients with HFO.....so the great advantge showed by HFO was our inappropriate management of conventional ventilator settings. I am not saying HFO is killing now our patients, but I am pretty sure we were killing our patients with mechanical ventilation, so HFO seemed a magical rescue treatment. Perhaps, I am wrong, but I think that alveoli does not care which device and mode are we using to open and keep it opened...if we use it properly.
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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?
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In our institutional experience, when the biopsy is done for a patient who is in an outpatient setting it usually provides useful information and a therapeutic change for over 50% of the patients. For critically ill and mechanically ventilated patients that require high PEEP and FiO2, perhaps it is too late and surgical intervention not only adds insult to injury but also doesnt change much in terms of therapy. Our mortality rate for outpatients is 0% and for ICU patients jumps to 45%.
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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?
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Hi,
This is a vey interesting question.
I wiil read the mentioned papers.
Kind regards,
Prof dr Johan (JT) Theron Nel.
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What are the common methods for recruitment? Are sigh, SI and e-sigh very commonly used?
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One basic maneuvers in ARDS patients should be to verify the diagnosis. Besides bilateral infiltrates and the pO²/FiO² index cardial reason should be excluded. PCWP < 15mmHg was part of the old ARDS definition. Recent Berlin ARDS definition skips the Swan-Ganz-Cath because it is not routinely used anymore. Instead, this new definition requires that the respiratory failure cannot be explained fully by cardiac failure or volume overload. ALI is removed by ARDS now divided into three categories based on severity of hypoxemia. PaO2/FIO2 between 200–300 is defined as mild
between 101 - 199 as moderate PaO2/FIO2 of less than 100 is defined as severe. Minimum PEEP level should be above 5mmHg. So far I prefer to adjust respirator settings to the FiO2 / PEEP table of the ARDS Network trial and early prone positioning in my ARDS patients.
Recuitment maneuvers have no clear standing in my point of view. So far there is no evidence that these tools are beneficial concerning outcome parameter. See the good review of Guerin et al. concering "Efficacy and safety of recruitment maneuvers in acute respiratory distress syndrome" (Ann Intensive Care. 2011; 1: 9)
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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?
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The problem with treating ARDS using mechanical ventilation is that treatment starts too late in the disease process. We have recently published two papers in a high fidelity clinically applicable animal model showing that preemptive application of the appropriate ventilation strategy actually PREVENTS ARDS. In our first paper (Roy S et al J Trauma 2012) we tested early application of airway pressure release ventilation (APRV) using very precise settings immediately post injury (peritoneal sepsis plus gut ischemia/reperfusion) and showed that we could prevent the development of ARDS. In the second paper (Roy S et al Shock 2013) we compared preemptive APRV with the standard of care ARDSnet low tidlal volume (Vt) ventilation, which was applied late after injury developed. Again APRV prevented ARDS while the low Vt did not stop disease progression and all animals in the ARDSnet group developed established-ARDS. Our efforts should not be at treating established ARDS because it is refractory to treatment. In the recent ALIEN paper by Villar he showed even with low Vt ventilation mortality is still greater than 40%, clearly showing that low Vt is not very effective. Indeed, nothing is very effective at treating established ARDS therefore we must attempt to prevent the disease from occurring. In the paper by Roy et J Trauma we discuss ARDS being a staged disease similar to cancer and the key to reducing ARDS mortality is application of treatment in an early ARDS stage, similar to reducing mortality for cancer.
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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.
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Good point Dave. And another benefit of applying protocols consistently is that we can learn from our mistakes and evolve better protocols. That is how artificial intelligence was able at last to beat humans at chess. The way we practice medicine now, by word of mouth, it is very hard to learn what works and what does not in a way that consistently improves patient care.
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Respiratory Physiology
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Yes! surely this is precisely one of the mechanism for the resistant hypoxaemia.