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Intensive Care Medicine - Science topic

Explore the latest questions and answers in Intensive Care Medicine, and find Intensive Care Medicine experts.
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For the acute resuscitation of adults with COVID-19 and shock, the current recommendations are suggesting, using buffered/balanced crystalloids over unbalanced crystalloids.
The purpose of this discussion is address the need for guidance on fluid resuscitation among severe COVID-19 patients and shock management in resource-limited settings
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Fluid management is a very complex issue.
There are many confounding factors including co-morbidities such as heart failure, liver disease and renal impairment.
It is important that management is individualised on a case by case basis.
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The study of ventilation during adult cardiac arrest remains challenging due to the unexpected nature of sudden cardiac arrest and the limited resources/personnel on site. This is especially true for interventions that influence outcomes when applied early in the cardiac arrest phase. Therefore, animal models (i.e. pigs, dogs), manikins, human cadavers and computer models have been used to study intra-arrest ventilation. Also, some data has been made available from registries and clinical studies in humans.
While the possible answers to my question heavily depend on the respective research question, personal perspectives on the well known experimental models, as well as lesser known models for this niche of cardiac arrest research, would be very much appreciated.
Please note, that I do not to intend to discuss airway management during cardiac arrest. Although, I'm aware that both intra-arrest ventilation and airway management are closely connected.
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Yet to be developed
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Different methods of recruitment are used to improve lung compliance and FRC. Which one you use for effectiveness?
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Different methods available for recruitment most commonly employed are...
1.High PEEP
2.Prone ventilation
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Participating in an ICU based study looking at intubated and ventilated COVID patients first out of bed rehabilitation session with Physiotherapists and trying to determine if it is safe by using group analysis to analyse physiological parameters such as systolic and diastolic blood pressure, heart rate and oxygenation. Currently very little data on what the MCID to determine how much of a change in these parameters would be clinically important that may determine if rehabilitation is safe for this patient group.
Any help would be greatly appreciated.
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The clinical significance of the selected parameters is related to the initial condition of the patient and the disease. Any sustained positive dynamics should be considered clinically significant.
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I'm doing a project on emergency team communication (in simulation). The data is videotapes, and I will do a turn-by-turn analysis of the talk.
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Thats really kind of you - thanks a lot
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what types of physical therapy protocols are used in the long term acute/critical care setting?
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You can see on North American Association of Neurology and Neurosurgery Guidelines
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The Health Technology Assessment (HTA) unit of the CHU de Québec – Université Laval is currently working to get data on integrated early rehabilitation interventions in pediatric intensive care unit.
We define «integrated early rehabilitation interventions» as physical, functional, nutritional, psychological, communicational, social or spiritual rehabilitation activities initiated during the first days of admission of a patient in the pediatric intensive care unit and delivered by each professional according to an intervention plan that has been developed beforehand as a team by these same professionals.
Are early interdisciplinary rehabilitation interventions an established practice in the pediatric intensive care unit of your hospital?
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Currently I am living in Bolivia and most of the Hospital don´t count with those services in ICU.
In Brazil there is a law that determine the presence of some of those professional (PT for example) 24/7. But that doesn´t translate into practice.
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In spite of the metaanalysis (Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares). Published in the
Chest. 2008 Jul;134(1):172-8.
Marik PE, Baram M, Vahid B, with the Conclusion:
(This systematic review demonstrated a very poor relationship between CVP and blood volume as well as the inability of CVP/DeltaCVP to predict the hemodynamic response to a fluid challenge. CVP should not be used to make clinical decisions regarding fluid management.) CVP may still the most widely used monitor for fluid management worldwide, do think that is true? Do you think it is accepted practice? And why?
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Interesting..
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NICUs are implementing care bundles to help decrease IVH in preterm neonates. The bundles start during the Golden Hour of resuscitation and continue the first 72 hours of admission. The bundle includes interventions to prevent fluctuations in cerebral blood flow, as a contributor to IVH.
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A good clinical study to explore, possibly by comparing pre and post implementation data, but also keeping in mind some other factors that may impact the outcome.
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I want to gather opinions about PACT modules by the European Society of Intensive Care Medicine!
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Thank you Rainer. Looking forward to any feedback!
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We described the proportion of lung contusion  in multitrauma patient that needs to be intubated or we can handle him other way (NIV, or other way etc) 
Management of 150 flail chest injuries: analysis of risk factors affecting outcome
Eur J Cardiothorac Surg (2004) 26 (2): 373-376.
Prognostic factors in flail-chest patients.
Eur J Cardiothorac Surg. 2010 Oct;38(4):466-71. doi: 1
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Dear Spiros,
thank you for sharing with us your research. Our project is not yet aimed at providing direct clinical recommendations, but rather at developing a technology to quantify lung aeration with MRI similarly to what is done with quantitative analysis of CT scans, but without ionising radiation exposure.
We are open to new collaborations and in case you are interested in assessing the possibility to join our efforts feel free to contact me in private.
Thanks again for your interest,
Lorenzo Ball
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Hi,
 First of all Sorry because, my question is not regarding research.
My mom got Acute respiratory distress syndrome due to viral pneumonia and now she is in intensive care unit by giving oxygen in high rate via BiPAP for more than two weeks.
I have attached  summary of medication with this question.
Doctor is providing high antibiotics and infection is under control.But she cannot maintain oxygen level without support of BiPAP even for short time. She is maintaining this situation with oxygen level of around 90  and for five days not showing any improvement. 
Doctor is saying that oxygenation for a long period is the only method to bring back original breathing. 
If any other medications available, can anyone reply?
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I am sorry to hear that this has happened to your mother. Hoping that she  will be better in near future. 
For the ARDS:
Ventilator aspects: recruitment maneuver, prone position ventilation, high PEEP
Drugs: diuretics, hormones, etc.
Extracorporeal Life Support: ECMO
Treatment of etiology: control of primary disease is very important.
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There are different results in literature for temporary abolishing of aspirin before TURP, neurosurgery and ocular surgery. The difference exist because lack of deffinitive guidelines in these situations. One should have in mind the difference between not only surgeries but also the fact why the patient is having aspirin th.; for primary oe secondary profilaksis?
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"Although aspirin increased the incidence of bleeding by 50%, it did not increase the severity or perioperative morbidity/mortality, except in intracranial surgery and, possibly, transurethral prostatectomy".(Burger W, et al.  meta-analysis. J Intern Med 2005; 257: 399–414.)
"found that aspirin (150 mg) continued in the perioperative
did not affect intraoperative blood loss but postoperatively
the blood loss in the aspirin group (median 284; quartiles 196–660
mL) was significantly higher than in the placebo group (median 144;
quartiles 75–379 mL, P = 0.011)".(Nielsen JD et al. The effect of low-dose acetylsalicylicacid on bleeding after transurethral prostatectomy—a prospective,randomized, double-blind, placebo-controlled study. Scand J Urol Nephrol.2000;34:194–198.
"Surgical procedures that involve particular anatomic locales (middle
ear, posterior chamber of the eye, intracranial, intramedullary
spine, and possibly TURP) confer the highest risk of complicating
hemorrhage while on aspirin therapy".((Ann Surg 2012;255:811–819)
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We´re looking to start measuring nursing workload in high complexity units. There´s evidence of the application of TISS - 28 in cardiac surgery patients but i´m not 100% sure if there is any incovenient to apply in other non surgical cardiac units.
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The limitations of the TISS-28 is it is based on how we provided critical care 20 years ago. A great deal of nursing care has changed since then that are not captured in the TISS-28. For example we keep patients more awake, promote more mobilization than before yet these items are not captured in the TISS-28.  I would argue, because it misses important advances in critical care, it has a tendency to underscore workload. 
Saying that, this tool does have a lot of validity and reliability evidence in ICUs around the world. 
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The very old (≥80 year) patients increases as well in the hospital as in intensive care. With ≈ 15% of all ICU admissions belonging to this group, this probably translates to at least 5-600.000 admissions in this group per year in Europe alone. The short and long term outcomes including mortailty is higher than in the younger one, which calls for:
  • improved prognostications & triage
  • improved treatment in particular post ICU rehabilitation
  • probably closer cooperationwith geriatricians
I would like to hear what you say out here, where do we have the unanswered questions regarding this issue?
Hans Flaatten
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Regarding the elderly patients there are some kind of problems in my opinion:
Among European nation there are some different ethical problem regarding end-of-life decision, religious and economic issue. Therefore there is an organizational problem, it is different when patient is admitted to ICU in an University Hospital or in a Community one. Then there are clinical issues elderly patients admitted to ICU after elective surgery have a better early and long term outcome than elderly admitted for unplanned surgery or medical problems. So, maybe, would be necessary a sort of score which can help physicians to chose for admitting elderly patients in ICU.
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What is your daily routine?
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It depends if the patient is mechanically ventilated or spontaneously breathing. Beside the clinical signs of dehydration, leg raise test associated with change in pulse pressure or cardiac output (by CO monitor or echo) is a good test. Most studies define fluid responsiveness as increase in CO/SV by 10-15%.
In mechanically ventilated patients, we use the heart-lung interaction and positive pressure ventilation, either by IVC assessment by echo (collapse more than 12%) or stroke volume variation (LIDCO). PICCO also is of great help.
Fluid responsiveness is a dynamic test and should be repeated through the management till the shock state had been resolved.
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I am undertaking a systematic review and have the following data for an outcome of interest from one publication (after multiple logistic regression):
Group 1 n=53,482. OR 1 (reference)
Group 2 n=38,077 OR 2.23 (95%CI 2.05-2.42)
Group 3 n=1,597 OR 1.18 (95%CI 0.86-1.61)
Group 4 n=1,916 OR 2.80 (95%CI 2.28-3.43)
I am trying to compare ORs of groups 2 and 4. The 95%CIs overlap, which raises the possibility of them being non-significantly different from each other.
Is there a reasonably straightforward way to calculate a p-value for this, from the data provided above?
I have access to STATA but limited experience so far.
Many thanks!
Johannes
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you may try the comparison of the ROC of the two groups you want to compare, but they may appear quite similar according to the lower 95%CI. Bonferroni correction is not required for a comparison of two populations.
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During  our  Post  graduate  training we  had  been  under  the  impression that  Fever  is  the  Most  difficult symptom  to  solve  and  fever  does  not  kill  the  patients  but  it  can  kill  a  Doctors  reputation,  But  here  the  story  comes :  In  early  2k,  I  was  on  duty  as  Assistant  Professor in  Medical  wards  of  a  reputed  Medical  college - Govt. Stanley  Medical  College,  in  Chennai - India. At  about  4  pm  my  Post  graduate in  Medicine  admitted  an  Young  27  years  old  female  with  an  history  of  fever  since 2  days.  She  delivered a baby  about  a  week  ago (  Full term  natural  delivery  and  smooth  ante-natal history). She  was  breast  feeding  the  baby. History  and  physical  examination  were  unremarkable.  I  was  angry  with  the  post  graduate  for  hospitalising  a recent puerperal mother  for  a  short  acute  febrile  illness without any  significant  physical  findings. About  an  hour  later  I received a  call from  the  post  graduate that  She  became seriously  ill  gasping  for  breath  and  rapidly  desaturating  in  the  ECG  room  while  an  ECG  was  recorded .  I  became  very  furious  towards  the  attitude  of  that  postgraduate  for  sending  the  patient  for  an  ECG,  which  I  thought  was  an  unwarranted  test  in  a  febrile  patient.  She  was  shifted  to  M-ICU  intubated  and  cardiac  resuscitation  was  attempted. In  vain.  She succumbed  to  the  undiagnosed  Acute  short  febrile  illness.  But  the ECG  was  very  diagnostic  in  determining  the  cause  of  death. Following  this  experience  until  now,  I  order  an  ECG  for  every  febrile  patients.
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Dear Muralidharan R.s.,
It is really a very sad story.
Since the topic is so interesting I have copied some important text to shed light on this kind of illness:
Acute febrile illness is the medical term used to describe a sudden fever or elevation in body temperature. This happens when the body is invaded by a pathogen and the immune system is activated to fight it off. Read more to learn about the symptoms and treatment options.
What Is Acute Febrile Illness?
When the body is invaded by a foreign pathogen like a virus or bacteria, the immune system kicks into gear and tries to fight the infection before it has a chance to spread. When this happens, the body's temperature is elevated to try to kill off the pathogen, and this results in what we call a fever. Acute febrile illness is when a fever develops suddenly; specifically, the body temperature rises above 37.5 degrees Celsius (99.5 degrees Fahrenheit).
Causes
If you've ever been sick, you've probably experienced having a fever, and you know how hard it can be to determine the underlying cause. Acute febrile illness can occur whenever the body is invaded by some type of infectious disease, but it is especially worrisome in tropical and sub-tropical regions where serious diseases loom. These can include malaria, dengue, typhoid, chikungunya, Leptospirosis, scrub typhus, influenza, encephalitis, histoplasmosis, enteric fever, rickettsiosis, Hantavirus, and many, many others. Specifically, the hypothalamus is the part of the brain responsible for regulating body temperature, and it may 'decide' to elevate body temperature in response to an infection.
Symptoms
In addition to causing elevated body temperature, acute febrile illness can be accompanied by headaches, dizziness, sweats, chills, muscle pain, joint pain, and weakness. Sometimes it's also affiliated with respiratory symptoms like coughing or wheezing. A fever in itself isn't necessarily cause for alarm; however, it becomes problematic when the body temperature gets too high or lasts for an extended amount of time.
In infants or very young children, fever may be accompanied by seizures (called febrile seizures). These are generally harmless (although they can be very scary to witness), though it's recommended to take children to the doctor the first time they experience a febrile seizure. They can be recurring, so it's best to make sure they aren't indicative of a more serious cause.
Rafik
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Quality Improvement group trying to improve care of deteriorating patients and deliver cost effective safe care in a large teaching hospital in the UK. 
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The above links are two examples of studies conducted in Australia to determine the effectiveness of an organised response to clinically deteriorating patients in hospitals.  They may add something to your inquiry.
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As lung protective strategy you prefer volume control or pressure control ventilator mode?!
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PC protects from high airway pressure. Lung damage comes from high trans-alveolar pressure, which may happen if there is a large inspiratory effort (ie, Pmus adds to Paw). We are talking about simple, set-point targeting of PC modes. You could choose to use adaptive targeting in PC (eg, PRVC or VC+ modes). It all depends on what your goal is. There are only 3 goals of ventilation, safety (gas exchange and lung protection), comfort (patient-ventilator synchrony), and liberation (minimize time on vent). The choice of mode, not just PC vs VC depends on your assessment of the patient's need and hence your clinical goal. There is a rational approach to selecting modes. See attached paper.
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During controlled mechanical ventilation as compared to spontaneous breathing, less gradient of pressure in the system exists helping with repetitively opening and closing of the alveoli. When lungs are ventilated e.g. using the positive pressure mode, by application of positive end expiratory pressure (PEEP) it prevents alveolar over distension during cycles by avoiding its repetitive opening and closing. The systemic venous blood return still depends on a pressure gradient between the extrathoracic veins and the RA (the right pressure gradient) to create adequate RV preload, but with lesser amount....(can this be quantified, and how?). AM I COMPLETELY WRONG by saying that: during controlled mechanical ventilation the inspiration does not significantly increase this gradient to the level as observed in case of spontaneous breathing to accelerate venous return while enhancing the preload? 
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cut off value of short, intermediate and long ICU stay 
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thanks a lot for your generous response Dr Dimitrios and Dr Stany.
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I am creating a bathing protocol using CHG in our Cardiac Surgery ICU. Please  share with me your practice since CHG is now globaly uses as antiseptic solution. Thank you
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we are using betadene scrub bath for the purpose
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My research project is looking at the levels of anaesthetic in artery (ug/ml), vein (ug/ml) and oxygenator anaesthetic gas level (%).
Theoretically, all the 3 compartments should be the same under equilibrium state.
Please correct me if I was wrong. Bland Altman plot is not applicable as part of statistical test because of different units % and ug/ml. My lab is not feasible to create a calibration curve for me to convert the % to ug/ml. I just have to accept the results given by lab. 
I would like to check if there is any correlation between these 3 variables. What types of statistical test would you recommend?
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While correct in concluding that Bland-Altman is not appropriate, I'm still not sure your reasoning in strictly correct.  Even "theoretically", the 3 compartments will probably not be in equilibrium. You might want to review your respiratory physiology notes, particularly the notion of ventilation-perfusion (VQ) mismatch. Imagine a blocked alveolus, which sees no gaseous isolflourane (V = ventilation = 0). There is still arterial blood flow (Q = flow  > 0), but it will not equilibrate with the inspired isoflourane. This happens to lesser degrees even in normal lungs, where VQ mismatch results in blood that is not equilibrated with inspired O2  return to the left heart via the pulmonary veins, which will now have a lower concentration than the alveolar gas. Depending on the gas (oxygen, CO2) and the corresponding solubility of the alveolar-capillary barrier, it may also contribute to lack of equilibrium. But in any case, you can't test for equality between them, since they are fundamentally different quantities. If you only had two variables, you would use some form of correlation coefficient for continuous variables. In fact, with only 3 variables, you might simply report pair-wise correlations (arterial with inspired, venous with inspired, arterial with venous), as long as you adjust for multiple comparisons. 
But I suggest you pick up a good text on the biostatistics and read about inter-rater agreement when the > 2 outcomes are continuous numeric. The 2005 Encyclopedia of Biostatistics (Wiley) has a brief (14 pages) chapter by Shoukri on "Agreement, Measurement of" that states:
For interval or continuous scale measurements, we estimate interclinician reliability with the “intraclass correlation coefficient” (ICC)
The "class" in this case is the subject being studied and the "clinicians" or "raters" are the 3 different measurements (this is a bit confusing, since we're not really looking at agreement here, but the analogy should be clear :). In your reading, you will discover that there are actually 6 different types of ICC depending on your specific experimental design. I think it would be good for you to try to understand which best applies to your trial before asking this list. The distinctions are important, and you will be able to ask a better question if you first understand your experiment. 
Atul
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Atul Sharma MD, MSc, FRCPC, M.Stat
Senior Consultant | Biostatistics Group | Data Science Platform
George & Fay Yee Centre for Healthcare Innovation
University of Manitoba
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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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I, an anaesthesiologist from India, presently working in Ireland have created a platform for discussion on relevant academic topic, interesting cases and controversial issues related to anaesthesia, intensive care and pain management. If you feel it is worth to share and gain knowledge, please join the "Anaesthesia Interactive Group" having 11,000+ members with vibrant academic activities which is more than 5 years old. 
To join the group please click this link "https://www.facebook.com/groups/Anaesthesiainteractivegroup/" and then click the "Join the group" on the right top hand corner of the page. Make sure to make your speciality, area of interest and practice in the public profile so that all members and Admins can know about you. 
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What is this going on sir? These really don't suits you to you guys .You both have given lots of things for our anaesthesiology. Please don't ....
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There is much discussion on this field, glutamine is recommended when critically ill patients need parenteral nutrition. We agree with this recommendation and use glutamine in our patients when parenteral nutrition is indicated.
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Glutamine is the most abundant free amino acid in the body, but its stores are rapidly depleted during critical illness or injury, including burns. Critically ill patients often have decreased glutamine level on ICU admission, and low plasma glutamine levels are associated with increased mortality.
However, the recent REDOXS trial showed a dramatic increase in mortality rates with high doses of enteral and parenteral glutamine (0.6 g/kg per day). Even though there were more patients with three or more organ systems (including renal failure) failing in the glutamine group than in the control group, a strong trend toward increased mortality with glutamine remained after adjustment for this. In another study (van Zanten ARH et al. JAMA, 2014), high-protein enteral nutrition enriched with glutamine and ‘immune-modulating nutrients’ did not reduce infectious complications or improve other clinical endpoints versus standard high-protein enteral nutrition and may have been harmful as suggested by an increased adjusted mortality at 6 months. Therefore, it's necessary caution untill the mechanisms behind the harmful effects reported in the REDOXS study are better understood.
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Routine PPI use ('stress ulcer prophylaxis') is standard practice in some ICUs, however it has been found that as many as 40% of these patients continue taking the medication on hospital discharge, with the attendant risks of Clostridium difficile infection, community-acquired pneumonia and osteoporosis.
Our ICU is currently developing guidelines on postoperative care for cardiac surgical patients, primarily to provide a basic framework for junior doctors regarding routine practice in the absence of any specific indications/contraindications.
I am interested in hearing how people interpret the risk/benefit profile of giving, for example, 40mg IV pantoprazole daily, to post-cardiac surgical patients as routine practice. Should it be used universally, liberally, sparingly, or not at all for this purpose?
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Please check out the landmark article by Cook et Al in NEJM. It looked at the risk of developing stress ulcer in critically ill patient. In multivariate only two conditions increased the risk of stress ulcers mechanical ventilation greater than 48 hours and coaguloapthy.
The American Society of Health System Pharmacist publish the most widely accepted guidelines for stress ulcer prophylaxis. New guidelines are expected soon. 
Finally, please see the article H2RA vs PPI in JAMA 2014 By MacLaren and colleagues that found higher incidence of hemorrhage, pneumonia and CDI with PPI over H2RA. 
As a side note considering administration- PPI cannot be crushed and given via an NG tube. Special formulations must be used or IV. H2RA, however, can be crused. Using the oral formulation via NG tube can offer a significant cost savings. For example, oral famotidine is ~1/50th the cost of IV pantoprazole. 
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I am currently interviewing SCI patients for my research study and some report the lack of mouthcare in critical care as being particularly upsetting. This should be provided routinely as part of a daily care bundle, however these patients have had to ask for it - despite being non-verbal at that time due tracheostomy/vent.
I'd like to find out about practices elsewhere.
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I work in a residential facility with individuals who have dual diagnosis (MR and other diagnoses, i.e., CP; ASD; Blind; Deaf; Deafblind; Nonverbal, etc.) and I am the chair of the Dysphagia team.
The standard in our facility is to ensure oral hygiene twice daily (morning and night).  I, of course, do not feel that this is adequate; especially for those who have or are at risk for aspiration and aspiration pneumonia.  Our team directs that all individuals who are under the care of the Dysphagia team receive mouth care pre and post-oral consumption with pre-consumption mouth care being defined as "checking mouth for any foreign matter and clearing mouth of all debris as well as providing a sip of a cool fluid to ensure that the mouth is not too dry to consume" and post-consumption mouth care as full hygiene including tooth brushing.
I believe that a lot more needs to be done in the area of oral hygiene--people tend to forget that the mouth is one of the best places to start in decreasing the risk of aspiration pneumonia (as well as allowing a free water protocol to be put in place which I would not feel comfortable beginning until I knew that appropriate mouth care is being provided to all who reside in this facility).
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Seeking input from experienced centers, utilizing ICUs without walls and deploy intensivisists in the hospital wards.  How can we measure baseline effectiveness and what are the best outcomes to study?
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Lancet. 2005 Jun 18-24;365(9477):2091-7.
Introduction of the medical emergency team (MET) system: a cluster-randomised controlled trial
This study probably describes not how to do it. The event rate in many of the smaller hospitals was too low which dramatically reduced the studies power to detect any effect of ICU led rapid response teams.
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When randomizing patients to two different plasma transfusion strategies, it is important to make sure the coagulation test used to differenciate both groups makes clinical sense.
Would you use INR (not designed for non-AVK patients but very commonly used), TP or aPTT ratios (more complicated to use are different tests yield different results), or ROTEM or TEG (not evaluated outside the massively-bleeding patients, and not often available)?
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As a Trauma Surgeon there are ample data that support the early administration  of plasma and platelets  for the critically injured trauma patient.  This may not be relevant to the critically ill medicine patients.
Sadly none of the instruments/laboratory assays provide an adequate real-time picture of the patient's coagulation status.  Even from TEG and ROTEM have issues related to patients with depleted fibrinogen stores and more importantly cold patients.  Many critical care physicians failed to recognize that when a battery of coagulation tests  are drawn and sent to the laboratory the laboratory warms the sample to 37°C.  Trauma patients owe as much as 50% of the coagulopathy to hypothermia.
Consequently, the answer is clinical judgment.  As a clinician you must take into account the injuries with their estimated blood loss and the patient's temperature and premorbid complicating medical conditions to determine when to give plasma.  As a rule sooner is better than later and warmed is better than cold.
On a separate note we are currently using type A plasma in addition to AB plasma.   The safety of this has now been documented but originally stems from the use of uncrossed matched platelets which carry with them a significant plasma store.  I'm curious how many facilities have liberalize their use of type A plasma to expand the store of fresh plasma for their trauma patients?
Respectfully
John
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Is there a correlation between the number of days premature infant required mechanical ventilation increase chance of requiring or needing bronchodilator therapy?
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Thank you for the reply. I am doing a research on number of days neonatal infants received Albuterol treatments while placed on conventional vent versus high frequency oscillator.  If the mode of ventilation does play a role on these infants that require bronchodilator therapy. 
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Is there any risk of iatrogenic C1-C2 subluxation in case of transverse facial cleft patient intubations and operations? What if there is no vertebral anomaly visible on CT.
I would grateful if you can help me. It is very difficult to get any publication about that subject.
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Flexible Fiberoptic specially awake intubation (if applicable) is the safest.
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As described in literature, CGD usually complicates with frequent gram pos. (but not gram neg.) infections. Does anyone know about the severity (i.e. severe sepsis, septic shock, need of ICU administration) of these infections? And about treatment? How well reacts these patient to antibiotic treatment?
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Hi,
very nice reviews from Vinh, Lancet Infect Dis 11; Kuhns, DB, NEJM 2010 and Falcone Curr Opin Infect Dis 12. Watch out mainly from Gram (+) indeed but also mold infections and especially breakthrough fungi since those patients are under long-term antifungals.
See u,
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What's the most useful tool you rely upon to prevent yourself from making an error, ensuring that you've entertained all the important possibilities? Do you have a favorite saying or memory aid that you teach trainees? This could be for a specific condition (like the Hs and Ts of PEA) or a general approach to ensure you aren't missing something.
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Medical diagnosis is something more complicated than just to takeoff. Checklist are appropriate for repetitive situation requesting a stereotyped verification. Safe surgery checklist is a good example of it. You can find specialysed checklists addressing specific diagnostic situations: if you collect all of them, you'll have a big textbook in your pocket. A different approach is to focus on the situation leading to error and on the cognitive bias that can favorize errors. Mark Graber proposed a very simple checklist that can alarm you if you are in a situation at risk:  Graber ML, Sorensen AV, Biswas J, et al. Developing checklists to prevent diagnostic error in Emergency Room settings. Diagnosis 2014;1:223-31.
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Feedback devices seem to improve compliance to Guidelines in CPR. Are there any outcome studies proving improved outcomes (i.e. ROSC, admission to hospital) in humans?
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Dear Paul, I Think that Answer is YES! Look This Attachment:
"Depth, Rate of Chest Compressions During CPR Impact Survival in Cardiac Arrest" -  Febbraio 6, 2015
DALLAS, Tex -- February 6, 2015 -- The depth of chest compressions and the rate at which they were applied make a significant impact on survival and recovery of patients, according to 2 studies published in Circulation and Critical Care Medicine.
Contrary to popular belief, the studies showed that cardiopulmonary resuscitation (CPR) compressions deeper than 5.5 cm resulted in decreased survival, possibly because of collateral damage to other internal organs.
Previously, investigations and guidelines indicated that deeper compressions were better. The American Heart Association's (AHA) 2010 CPR guidelines recommend compressing the chest at least 5 cm without providing any upper limit.
“Most people do not recognise that it takes quite a bit of thrust to compress the chest 2 inches,” said Ahamed Idris, MD, by UT Southwestern Medical Center, Dallas, Texas. “About 60 pounds [27 kg] of pressure are required to reach this depth, but in some cases a burly fireman or well-intended volunteer can go way past that amount, which can harm the patient.”
The researchers also found that the rate at which chest compression was applied was most important. Compression rates of 100 to 120 per minute were optimal for survival when other factors were considered.
“Survival depends on the quality of the CPR,” said Dr. Idris. “Both the depth of chest compressions and the rate at which they are applied can have important results for patients in the first moments of cardiac arrest.”
About half of responders are giving chest compressions too fast, with about a third above 120 compressions per minute, and 20% above 140 per minute, said Dr. Idris.
The researchers will continue to oversee innovative clinical trials to test the early delivery of interventions for serious trauma and cardiac arrest as part of a federally funded consortium aimed at advancing prehospital emergency care.
The Resuscitation Outcomes Consortium (ROC) has enrolled tens of thousands of patients to test prehospital interventions to improve outcomes in severely ill or injured patients before they are transported to a hospital.
SOURCE: University of Texas Southwestern Medical Center
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There are numerous studies on Dexmedetomidine use in children, especially in relation to procedural sedation. Are there any newer drugs that are being studied for use as continuous infusion in PICUs? 
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I know your question was human based, but in vet medicine, we also use dexmedetominie for boththe sedative effcts as well as the analgesic effect. We recently have started suing very low doses of alfaxalone (alfaxlone in cyclodextrine) which seems to be better than propofol in termes of resp depression. In terms of pain in particular, we tend to use lignocaine and ketamine infusion, in addition (or not0 to opioids. Do you do similarly in human?
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Why not use a MULTIVIB mattress for transferring sound stimuli to these patients?
It can transfer music as well at VAT stimuli, and will aid the process of ventilation significantly.
Olav Skille
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For those of you who maybe interested in holistic medicine, some anaesthetist use in animal an acupuncture point which, apparently may help with ventilation: GV 24...but it seems they use to stimulate breathing during recovery from anaesthesia, while weaning from the ventilator...not sure it will halp in terms of increasing ventilation in an alrady breathing aptient.
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I see many anesthesia techniques can be used for kidney transplantation.
In my hospital for recipient we use lower combined epidural & intravenous anesthesia (TCI propofol). Postoperative analgesia achieved by continous ropivacaine 0.15% + fentanyl 2 mcg/mL, rate 8 mL/hr via epidural catheter for 3 days and iv paracetamol.
For laparoscopic living donor we use combined epidural & general anesthesia (volatile). Postoperative analgesia: intermittent epidural bolus (bupivacaine 0.125%, morphine 2 mg, volume 10 mL, 2x/day) + iv paracetamol.
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For renal transplant recipients, we use Epidural Anesthesia and use fentanil with ropivacaine 0,2% In PCA post operatively. For donor, we use thoracic epidural in conjuction with GA.
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Some notation: 
ECG = Electrocardiogram
RR = RR interval (the time elapsing between two consecutive R waves in the ECG; the interval from the peak of one QRS complex to the peak of the next as shown on an ECG. It is used to assess the ventricular rate.)
ICU = Intensive Care Unit
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I have two instruments in ICU measuring the RR intervals for some patients.  So I have, for a single patient, 2 discrete series of RR intervals with hundreds of values:
RR1 = (823, 825, 884, 830, 900, ...)
RR2 = (843, 835, 874, 820, 910, ...)
I want to know if the two instruments are giving statistically equivalent measures, i.e., if I can use one or another instrument.
I am convinced that I must us statistical techniques to evaluate the reliability and the agreement. Bland-Altman and limits of agreement, Lin's correlation coefficient, but I think I must also use ICC, but which one?
I appreciate if anyone could help me with this or with another ideas / suggestions.
Thanks a lot.
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Dear Paulo:
ICC, CCC and Bland-Altman are methods to assess reliability with continuous data.
CCC is identical to some ICC.
ICC has several advantages: global assessment of reliability since it combines both bias error and random variation into a single coefficient; besides that, it is possible to evaluate the agreement when there are more than 2 raters.
The main disadvantage: ICC is quite affected by the heterogeneity of the sample and commonly shows very high values that may be biased (In a recent study, we found ICC values of 0.58 -first tertile-, 0.28 -second tertile- and 0.46 -third tertile-, whereas ICC on the complete series was 0.90!!)
The Bland-Altman plot is a good method to know the distribution of differences, the heterokedasticity, limits of agreement and repeteability coefficient.
My suggestion is the use of both the ICC and the Bland-Altman method.
Regards.
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8 kg, 10 month old baby with a type I Chiari malformation.
This is a new procedure for our anesthesia department to be managing and I am looking for any advice/direction that would be helpful. Thank you.
Suggestions for links to articles?
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We do not have such a small age of Chiari malformation undergoing surgery but we do perform about a dozen cases from 1994 in our hospital, often with correction of scoliosis. Smallest age is 13 y.o.. No particular attention for us, anesthesiologist, although a theorical difficult airway and M.H. incidence...thanks God we do not encounter although I remember one of them has a combined Klippel Feil and Sprengel deformity. None of them have CV abnormalities. Complications encountered are: CSF leak, meningitis but no fatal outcome..   
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In critically ill patients, they may show some endocrine dysfunction. Waht test is useful in these patients?
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You should specify which patient are you talking about (i.e. neurologic, septic, etc.). In general, there is no need for endocrine tests unless history and the clinical condition suggests a specific deficiency. Even in septic shock, low dose steroid treatment can be initiated without the need to test for adrenal insufficiency (see FunkD. et al. Low-Dose Corticosteroid Treatment in Septic Shock: A Propensity-Matching Study. Crit Care Med 2014; 42:2333–2341).
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The use of pre-blood fluid in the reduction of filter clotting in dialysis is well known, but it is also known to reduce the efficiency of the dialysis abilities.
Could you please explain how your unit overcomes the drawback of the use of pre-blood fluid, and how the use of Filtration Fraction determines the use of pre-blood fluid? Some units determine that pre-blood fluid is not needed if the Filtration Fraction is below 30%. 
Does this not then save the unit money if pre-blood fluid is not used? Also, it has been stated that in the use of Heparin in Dialysis, the APTT is irrelevant in the ability to stop the filter clotting off. What APTT therapeutic range does your unit run at?
Any information provided would be appreciated.
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Thank you Ali for your input on this subject, I will read them with interest.
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Dexmedetomidine is used as an adjuvant to intrathecal  local anesthetic                     (Bupivacaine/ Ropivacaine ). Does it help in prolonging duration of spinal anesthesia? How would you rate it on comparison to fentanyl/ morphine?
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Have never used it, coz this is the place where it can be carried to CNS and its vital tissues directly. However, in the epidural route and peripheral blocks the absorption characteristics are variable. But free accessibility of this drug to CNS structures while floating in CSF has not been studied extensively and mainly Indian studies are available only. Even the dose calculation is little weird when it is used intrathecally. Concerns from FDA are likely to come up soon regarding its intrathecal use.
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I am working on a better system of tracking and cycling IV pumps through central sterile supply and can not find information concerning the cost per pump that is an industry standard (B. Braun Infusomat Series) or the general needs per patient in a Medical ICU, Surgical ICU, PICU, or Post-anestesia units.  Any advice would be appreciated. 
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I think, central pumping has its own merits and demerits. Especially for critically ill patients, therapeutic approach is individualized and as such setting central pumps will prove very costly particularly in ICU. Can be considered in general wards but sill i think initial cost will be very high and their potential utility in long run also depends upon so many clinical and economical factors which can prove to be limitation for such a costly set-up
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Are there any specific number of these procedures you need to perform under supervison to achieve competency? How many you need to do to maintain this competency?
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 Not so dificult,.In our depatrement anesthesiologist to do percutaneous tracheostomy. I agree- 5-10 supervised is enough to independently work.
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In my country some high E:N enteral formulas are fiber-enriched. Some colleagues have concerns in prescribing these kind of formula in critically ill patient, even if these patients achieve hemodynamic stability. I would like to know the experts practice.
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The debate about feeding and haemodynamic stability is totally superfluous. Most often when patients are unstable, we are concerned with resuscitating them and often the gut is forgotten! We only think about the gut as a 'secondary organ system' and when we have 'resuscitated' the patient and can step back, do we think of nutrition! But what is resuscitation? Is it a set haemodynamic end points? Is it normalisation of acid-base status, normal or near normal pulmonary gas exchange (i.e. a near normal PO2) or return of urine out put? So, in my view the debate should not take place at all. Sick patients (as we see them in ICU) are more often than not nutritionally challenged as they may not have eaten for a few days (at home) or not been fed on the hospital floor before ICU admission. Either way, feeding (high fibre or not) IS PART OF HOLISTIC RESUSCITATION of the patient!
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I'm looking at the use of Citrate in CVVHDF in the critically ill patients with and without AKI. Do other healthcare professionals endorse it's use or discourage the use of citrate over heparin?
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We have been using citrate (first, homemade concentration of 30%) for more than 10 years (right now citrate 4%for compliance with european regulations purposes) with efficacy and security, provided nurses and junior doctors receive prior teaching. Heparin systemic administration is parallelled only in specific cases (ECMO..).
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We have performed a study about the knowledge of evidence based medicine (rating) among anesthesiologists and students.I am not familiar in this topic we have asked 90 doctors and 40 students to rate 40 papers by EBM classification. I do not feel that we have the best conclusion. If you are good in this field I send you more infos y mail.
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Be glad to help. Let me know.
Allen
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Based on your personal clinical experience in your field (Neurosurgery, Anesthesiology, Neurology, Pediatrics and etc.)
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The question is Mannitol versus Glycerol?
Why not Hypertonic saline ??
The benefit of Glycerol on acute stroke is not well established, its benefit on acute brain traumatism injury remains questionable, however some have recommended it’s orally use after a mannitol challenge.
In contrast to Glycerol, Mannitol benefits are evident, and thus WAS CONSDERED as the gold standard.
Recently, its detrimental effect of on mortality when compared to Hypertonic saline has been highlighted (Cochrane 2013), thus we may prefer sodium lactate (Ichai C et al ICM 2009)
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During our studies we have met a problem using nomogramms by Kelman and Nunn. According to their data there is the same correction line at all saturation levels below 80. This should be wrong. At least the values gained for mixed venous blood does not seem to be correct.
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Il mio piacere!
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The article by Nielsen et al, November 17, 2013DOI: 10.1056/NEJMoa1310519 questioned the effectiveness of hypothermia in this situation.
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Normothermia 36ºC should be the end point after cardiac arrest based on the most precise RCT performed till nowadays (TTM trial).
N Engl J Med 2013;369:2197-206.
The question could be...should we cool all our patients after cardiac arrest or only those whom present temperature above 37ºC...?
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Some colleagues claim that inserting a central venous catheter without ultrasound help is a vicium artis. Still, most of my colleagues and I mostly use anatomical landmarks. If several such attempts fail or we have a history of prior fail attempts, we use the ultrasound.
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So I pose the question..
Without US, how can you determine;
1) the vessels patency
2) the vessels pathway
3) respiratory variation/haemodynamic stability of the vessels
If you had a thrombosed R)IJ, then you would not know until you had already tried the procedure i.e punctured the vessel (on possibly more than 1 attempt, and had a likely failed guidewire feed).
US would allow the clinician to determine the vessels 'state of health' before even commencing the procedure, therefore reducing the risk of possible inadvertent thrombus dislodgement.
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Can anyone tell the negative airway pressure in the trachea during inhalation, during calm respiration but also in a forced deep inhalation, model human 60 - 80 kg?
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hi karen,
interesting question ...
i don't know how detailed you want/need to know this. as far as i remember according to typical physiology books: normal intrathoracic negative pressures during spontaneous respiration are between -5 to -20 cmH2O, and i assume it will be similar in the trachea, however, i do not know the exact pressurue gradient lowering this value in the trachea, apparently it has to be higher than in the alveoli to keep air flowing. however in obstruction maximum numbers such as -140 cmH2O have been observed.
christoph
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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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In our unit (a tertiary care, referral center) a review over a 2 year period revealed the incidence of UVC extravasation to be 4.2%. The most common mode of diagnosis was ultrasound of abdomen with the following features.
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I am surprised with your results.! Which persons (nurses, interns, paeditricians or neonatologists) in your NICU staff are responsible for setting UVC? Do you have a control group (infants without UVC)?
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In patients with cardiac arrest from accidental hypothermia patients should be transported during ongoing CPR to a hospital with ability to perform "bypass" rewarming.
Most in-hospital deaths in this group is probably because rewarming does not lead to spontaneous circulation, but data is scarce. However, patients may also die after successful rewarming with return of circulation. We have experienced death several days later from sudden development of cerebral oedema and tamponade. This has led us to question the common practice of rapid rewarming to normothermia and extubation.
Should we expand our ICU treatment by controlling the temperature for 2-3 days, aiming for temperature target 34-35 oC and sedation/controlled ventilation before "waking" up? Should we increase the level of neuromonitoring as a routine in the ICU in such patients?
What are your experiences (if any) and views?
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Dear Hans
I hope this part be useful for you ...
Many hypothermic patients have severe infections or other life-threatening illnesses. Patients with "uncomplicated" hypothermia (often due purely to cold exposure) have a fairly low mortality rate; patients with significant associated diseases have a much worse prognosis. ln terms of ultimate outcome, the underlying disease process is far more important than the initial temperature or the rewarming method chosen.
Therefore, evaluation and treatment must include a search for associated diseases as well as management of the hypothermia itself.
If asphyxia or near-drowning precedes the development of hypothermia, the prognosis is very poor. If asphyxia has not occurred, the protective effect of hypothermia may have an important influence on prognosis. Decreased oxygen requirements can protect the brain and other organs against anoxic and ischemic damage. This means that the usual criteria indicating death or irreversibility of disease are not valid in the hypothermic patient, who may even survive prolonged cardiac arrest without neurologic sequelae.
Tintinalli's Emergency Medicine(2011), Section16: Environmental Injuries, Chapter203: Hypothermia, Page 1338.
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We have one completed retrospective data collection and analysis on particular Health indication. Now wanted to published it in index journal.The scientific and ethical approval already has been taken. Can anyone guide me step by step to approach to draft synopsis and research paper/ article. You may provide format if any . It would be great support for me.
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Usually journals want to get the full article at once: the abstract will be a part of the full article. Also, every journal has its own standards for abstrats: is some the length is maximum 100 words, in some, 250 words, some journals want to get a 'structured' abstract (the aim, data, results and implications all separately). So, you still need to find a suitable journal and then read its instructions for authors (every journal has its own instructions, and they can be very different: allowed paper length, the way how to format the list of references etc. can differ a lot). Also, look at the papers published there: what their authors have written in their abstracts.
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What is your recommendation?
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Foreign body aspiration (FBA) is one of the main causes of accidental death in childhood. Most studies show that fewer than 15% of foreign body aspirations occur among children older than 5 years of age. Boys comprise more than 50% of all cases of foreign body aspiration. It’s largely preventable, and the morbidity and mortality associated with it can be significantly reduced by public education (especially parents, caretakers and families) and legislation.
Educational campaigns carried out through television and radio broadcasts, articles, and interviews in newspapers especially vernacular newspapers and educational programs at pediatric outpatient departments and wards using audio visual aids can increase community awareness about the dangers of FBA.
Most importantly, physicians and health workers can play a significant role in spreading awareness about FBA in the community. Sensitizing the community toward the need of awareness regarding FBA through educational campaigns involving mass media and stricter measures if taken by the primary care givers can drastically reduce the morbidity and mortality associated with FBA.
I am pleased to share this link with you.
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Major trauma patients in ICU often require aggressive fluid management. However overzealous crystalloids/blood transfusions have associated problems. Central venous pressures and arterial line waveform are not always helpful in determining need for fluids. What is your experience regarding use of Ultrasound/Echocardiographic imaging of IVC diameter changes in assessing fluid needs of these patients.
Attached is a link to online pdf of the article "Barbier C et. al. Respiratory changes in inferior vena cava diameter are helpful in predicting fluid responsiveness in ventilated septic patients. Intensive Care Med (2004) 30:1740–1746".
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As an Emergency Physician i find it a very useful device to have and effective in fluid depleted patient requiring critical resuscitation .
The key is expertise in scanning as always error of judgement is there as it i soperator dependent .
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Niccomo -the combination of impedance cardiography (ICG) and peripheral impedance plethysmography (IPG).
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I don't have experience using Niccomo, but I have some using Nicom which is similar. I think that it could be a good monitoring for typically anesthetized patients but not really for septic patients. Indeed, the analysis is based on the amount of fluid in the thoracic cavity, which varies a lot during resuscitation of septic patients. Moreover, I am quite sure that you are inserting arterial and central venous lines to treat your septic patients. So, once you've already inserted those lines, why not use a more invasive monitor like Picco or another thermodilution monitor which is definitely more precise?
To conclude, I think that Nicom or Niccomo are good monitors when you really need a minimally invasive monitor like in the OR.
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I have heard of people using APRV, which seems a little odd in the absence of inspiratory efforts. My impression is that there is not much research on this topic. Any thoughts?
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Accordingto the data published by Mascia (JAMA, 2010, 304, 2620),we use volume control ventilation with VT 6 to 8 mL/Kg, PEEP 8 to 10 cm H2O (according to the hemodynamic tolerance and respiratory mecanics (we use the stress index). We use CCS for trachal aspiration and performed the apnea test in CPAP. RM were performed after each disconnection.
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PDE-3 inhibitors, like Enoximone, increase cardiac index in some scenarios. Their application usually lowers systemic vascular resistance (SVR) which can lead to a higher cardiac output. I would like to know how much of the effect of PDE-3 inhibitors really bases on sth. like positive inotropy and how much of the effect is a result of decreased SVR (and so could possibly eaten up by the use of noradrenaline).
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I'm a cardiac anesthesiologist and my expertise is in the field of cardiac surgery. My experience with PDE3 inhibitors has been changed over the time. In the early 90' the scenario in our adult and pediatric intensive care units was completely different from the actual one. Patients in those years tipically come out the operating room extremely cold because of the hypotermic arrest with systemic vasoconstriction with very high SVR and low CO. We had the idea that much of the effect of Amrinone or Enoximone on CO was due to their vasodilatory effect. Still then it was possible to note some difference between that drugs being Amrinone much more a vasodilator than an inotrope while the inotropic potential of enoximone was much more evident. However time goes by and fortunately surgery technique has been changed, ECC has been developed and also patients and their preoperative therapies are different from those we had in that time with much more betablokers and ACE inhibitors use. Therefore the scenario has been profoundly changed and now we tipically have to treat patients with normal or low or very low SVR and sometimes low CO. Now I can say that enoximone is really a good inotrope independently by its vasodilatory effect. Nowadays the systemic vasodilator effect of enoximone and the consequent hypotension is quite an adverse effect that we usually have to counterbalance it with vasoconstrictors. In my actual experience norepinephrine is most used to avoid excessive hypotension in an abnormally vasolilated patient, expecially during bolus infusion and is often needed. In conclusion I believe that the effect of Enoximone on CO derives by its own inotropic effect. In vasoconstricted patients however an indirect effect driven by dilation has to be considered. To note that in patiens with isolated right heart failure with high pulmonary vascular resistances PDE-3I have the best effect. In those patients the dilation of the pulmonary vascular bed toghether with the direct inotropic effect on myocardiocyites produces a great improvement of the right cardiac output as it is typically seen by TEE and if the left ventricle is normal or quite normall we usually observe a global improvement in cardiac performance without hypotension.
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In mechanically ventilated patients, how often and how do you deduce the PEEP value while monitoring central venous pressure via central venous lines? One way, that I have been taught, is to subtract the PEEP value above 5 from the actual measurement of CVP. Does this hold true for patients with ARDS or with widespread alveolar/interstitial disease?
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As Stephen Lapinsky correctly states the contribution of the PEEP to the value of the CVP depends on the compliance of the lungs, and unless further montoring is undertaken this is unknown. Even oesphogeal pressure ( difficult to do and interpret) may not reflect the "global"transmission of PEEP to the venous return.
However if the CVP response to fluid challenges are followed, it is possible to detect the point at which further fluid results in rapid rises in pressure , suggesting the steep part compliance curve have been reached. This pressure differs between patients , over time and with PEEP. A rise of > 5cm H20 ten minutes after a fluid bolus of 500ml suggests further fluid loading will not improve the ability of the Right heart to increase cardiac output .
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I know it depends on many factors, however I need to know if awake fibreoptic intubation is your first choice in these patients, or if you do not use it at all, or something in between.
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For me, how often you use it depends very much on the criteria that you use to decide whether the patient is a candidate for awake intubation, in other words - patient selection. Fourth National Audit Project in the UK stated that awake intubation was not used when indicated in a number of cases that ended up as major disasters of airway management (ischemic brain damage, surgical airway, intensive care admission and death).
I agree that it needs to be practiced regularly so I suggest that fibreoptic scope should be used instead of Macintosh laryngoscope for intubation of any patient who is having general anaesthesia and requires tracheal tube placement for their surgery (providing patients have normal airway and are not aspiration risk).
So you would be using fibreoptic laryngoscope instead of Mac for intubation of a regular patient scheduled to have general anaesthesia and intubation. Although, acquired on anaesthetised patient, the skill acquired this way is likely to increase you confidence in using fibreoptic scope. One of the reasons why British anaesthetists don't use awake fibreoptic intubation often enough was to do with confidence in performing this procedure. This often led to more risky airway management options being undertaken with potentially serious consequences.
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If we dont have rapid EEG in the PICU can we use it ?
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Can BIS monitoring be used to assess the depth of propofol
anesthesia in the treatment of refractory status epilepticus?
*Tadeusz Musialowicz, yEsa Mervaala, zReetta Ka¨lvia¨inen, *Ari Uusaro,
Epilepsia, 51(8):1580–1586, 2010
doi: 10.1111/j.1528-1167.2009.02514.x
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Actually we have a patient of 2 y with RSE trated with midazolam propofol and thiopental
as rescue we use ketamine with good results ....
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Dear Raoul. ....
Thanks for your answer. We obtained a resolution of the RSE and we use the dose recomendad by Rosati
Actually the children is under ketogenic diet .
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I am having a look at the validity of the dynamic TIMI score as a predictor of one year mortality in my study cohort. I have a couple of questions:
The heart rate, BP and Killip Class - is this at admission? To my understanding the dynamic score is done throughout the hospital stay, unlike the Base TIMI which is at admission and then cannot be changed. At which point are these variables added to make up the dynamic score?
Also, one variable is if the patient is Anterior STEMI, why only this one?
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Found some good stuff after rooting around a bit. The baseline TIMI remains the same, the new variables (dichotomous) are added as an in patient
Open access article doi: 10.1161/JAHA.112.003269
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Do you use difficult airways algorithms and guidelines in your daily practice or do you have your own strategy? Which algorithm have you found preferable? Do you think current guidelines are simple and easy? Any recent updates?
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ASA published only recently their updated airway algorithm (Anesthesiology 2013; 118:251-70). Current algorithms (ASA, DAS) are very useful, but we found some of them difficult to follow in critical airway situations. We developed our own algorithm which starts with mask ventilation - the first measure the anesthesiologist will try if any problem occurs. We also included all the tools that are available at our institution. I attached a translated version of the algorithm. Any critics? Suggestions?
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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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Do you agree with performing a percutaneous tracheostomy without the aid of fiberoptic bronchoscopy?
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I agree with Palanikumar. Most of PDT in our ICU are performed with endoscopic guidance/control to reduce major complications like perforation of the posterior tracheal wall, bleedings, cartilage rupture or tracheal tube misplacement.
My second prefered technique especially in patients with short neck is changing to a laryngeal tube and puncture of the trachea with ultrasound guidance. Nevertheless after tracheostomy a bronchoscopic control is done to exclude above mentioned complications.
Although some groups claim that PDT is safe without bronchscopic guidance it increases patient's safety. If you have it - use it.
You can compare this discussion with the threat about ultrasound guided central venous cath introducing. Landmark guided insertion can be safe in experienced hands but ultrasound can decrease complication rate even more.
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What's your opinion about using Airtraq laryngoscope in emergency situations? Do you have Airtraq in emergency trolley in your hospital? As the first successful attempt is very important and sometimes life saving, do you use Airtraq as the first choice in cardiopulmonary resuscitations with anticipated difficult airway? What's your preference in difficult emergency cases?
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There is plenty of evidence suggesting that videolaryngoscipes are more successful at managing difficult airway (when difficulty is defined by limited view at Macintosh laryngoscopy). Choosing the videolaryngoscope that you have some experience in using in normal airways is important point mentioned previously as almost all videolaryngoscopes require some adjustment to your intubation technique.
I would disagree though with ILMA (Fastrach LMA) being selected as suitable device for use in failed intubation. This device has to be used with the guidance of fibreoptic scope if it is to be effective (UK DAS guidelines). A number of surveys in the UK pointed towards limited experience with this device. Blind intubation through the ILMA has a success rate of around 80% - not enough for a failed intubation rescue device. Fibreoptic guided intubation through ILMA has much higher success rate but requires significant amount of training before proficiency is achieved.
I would argue that learning to use a videlaryngoscope is much simpler and easier than learning to intubate through ILMA with fibreoptic guidance.
Use of Airtraq and Pentax AWS in the prehospital setting is now well researched and supports the use of these portable devices that are shock and water resistant to a reasonable degree.
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If a person is on a ventilator with a tracheostomy done and has developed ventilator-associated pneumonia along with other complications such as blood loss,blood pressure drop etc. and is in a semi-conscious state. The patient is lying stable but in a crippled condition with no signs of recovery. What are the chances of his/her improvement? "to what end" is it possible to keep the patient dependent on the ventilator?
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There is no precise limit. Some patients may survive for a long time. By and large the cause of death is infrequently respiratory failure , but MODS (multiple organ failure ) is the culprit. if no success in weaning from the ventilator, a tracheostomy should be performed relatively soon . Patients may remain ventilated for years (home ventilation) as long as no other complications arise
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Lowering body temperature during the first hours after cardiac arrest reduces neurologic injury by disrupting pathological cellular events and cascades that might lead to secondary brain injury. Randomized trials demonstrated that therapeutic hypothermia early after cardiac arrest reduces mortality and improves outcome. Based on preliminary results, it was postulated that a shorter delay to target temperature would further improved outcome. However, those early results were not verified in following randomized trials. Thus, the question if time or delay to therapeutic hypothermia matter in patients resuscitated from cardiac arrest...
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Dear Michael, dear Ingo,
thank you both very much for sharing your experience and your preliminary data. It seems more than important to perform prospective multicenter trials in this context. Regarding the possible confounders (e.g., baseline temperature, length of CPR, ...) it would be interesting to know how your results (Michael) are influenced after adjusting the multivariable analysis.
Once again - thank you for your contributions and best regards
Raoul
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For assessing sedation, what is the best tool?
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Richmond agitation sedation scale ( rass ) is an objectively corroborable and reproducible assessment tool under standarized conditions.
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Delayed surgery may warrant lower risk of residual shunt but pay an high risk of hemodinamic worsening also when IABP is promptly instituted. ECMO and MCS may warrant optimal haemodynamics to patients arriving to surgery in cardiogenic shock. Do we need to consider this escalation when IABP is not sufficient to delay surgery? When and how do we should revascularize those patients?
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In my opinion, the option to use ECMO when you meet a very unstable patients is very useful. I personally have treated some patients with huge posterior VSD (the worst type) after 6 days of ECMO. The aim is to buy time to remodel the haemorragic site of myocardium and to warrant a good operation with very low risk of residual shunt
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An otherwise healthy 54 year old female is admitted with acute abdomen. She is operated, and a colon cancer is found. A hemicolectomy is performed. Postoperatively she experiences rupture of an anastomosis with severe peritonitis and septick shock on day 3 after surgery. She is admitted to the ICU. Over the next weeks her organ dysfunctions gets worse with multi-organ failure (circulation, respiration, renal failure and several small cerebral infarctions). There is no improvement, and we withdraw therapy after 59 days treatment in the ICU after concensus with her family. She dies within 15 minutes.
What would you say about her death:
Sudden? Unexpected? Natural death?
Would you ask for an autopsy?
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Reviewing the termination of life support treatment, would you disconnect a mechanically ventilated conscious or semiconscious patient , probably begging you help? (Most probably this was the withdrawn treatment that killed within 15 minutes) I would like to review the definition of euthanasia according to BBC ethics guide as follow:
Active euthanasia
Active euthanasia occurs when the medical professionals, or another person, deliberately do something that causes the patient to die.
Passive euthanasia
Passive euthanasia occurs when the patient dies because the medical professionals either don't do something necessary to keep the patient alive, or when they stop doing something that is keeping the patient alive.
switch off life-support machines
disconnect a feeding tube
don't carry out a life-extending operation
don't give life-extending drugs
According to The British House of Lords Select Committee on Medical Ethics: It defines euthanasia as "a deliberate intervention undertaken with the express intention of ending a life, to relieve intractable suffering"
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Which considerations should be decided before admission in ICU?
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The need for intensive nursing care determines placement. If ICU nursing skills and the higher nurse staffing ratio are not required, the patient can go to the regular ward. In other words, think of the patient's nursing care requirements.