Science topic

Critical Care - Science topic

Health care provided to a critically ill patient during a medical emergency or crisis.
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How is the administration of vasopressors andinotropes optimized in critical care settings?
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We are inviting researchers and scholars to collaborate on a comprehensive narrative review focused on Critical Care. The aim and outlines will be shared with the selected contributors. We seek contributors who are passionate about Critical Care and can provide valuable insights through their expertise.
Requirements:
  • Background in CC medicine or nursing, etc.
  • Previous experience with writing is a must.
  • Proficiency in using EndNote is preferred.
  • Commitment to timely and quality contributions.
To express your interest, please send the following information to Ms. Hana Abukhadijah at HAbukhadijah@hamad.qa
  • Name
  • E-mail
  • Affiliation (Department, Institution, City, Country)
  • Critical Care experience (Yes/No)
  • ResearchGate (RG) profile link
  • Google Scholar profile link
Authorship: Authorship will be offered based on the timely and quality contribution of the collaborators.
We look forward to your participation in this exciting project and hope to produce a high-impact review that contributes significantly to the field of CC.
Best regards,
Abdulqadir
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How does hyponatremia develop in the critical care setting, and what are its clinical manifestations?
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How does continuous re-evaluation of monitoring techniques contribute to patient management in critical care settings?
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The title that i need to do in my study is Perceived Barrier toward Medication Errors Reporting among nurses in Critical Care setting.
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How does the role of anaesthesiologists extend beyond anaesthesia administration to encompass pain management and critical care services?The role of anaesthesiologists extends far beyond the administration of anesthesia to encompass a wide range of services, including pain management and critical care.
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The role of anaesthesiologists extends far beyond the administration of anesthesia to encompass a wide range of services, including pain management and critical care. Here's how anaesthesiologists play key roles in each of these areas:
  1. Anesthesia Administration: Anaesthesiologists are specialists trained in administering anesthesia for surgical and medical procedures. They are responsible for assessing patients before surgery, selecting appropriate anesthetic agents and techniques, monitoring patients throughout the procedure, and managing postoperative pain and recovery. Anaesthesiologists ensure patient safety and comfort during anesthesia induction, maintenance, and emergence, optimizing surgical outcomes and patient experience.
  2. Pain Management: Anaesthesiologists are experts in the assessment and treatment of acute and chronic pain conditions. They employ a variety of pharmacological and interventional techniques to alleviate pain, improve function, and enhance quality of life for patients with acute and chronic pain. These techniques may include medications, nerve blocks, epidural injections, spinal cord stimulation, and other advanced interventions. Anaesthesiologists collaborate with multidisciplinary teams, including pain psychologists, physical therapists, and social workers, to develop comprehensive pain management plans tailored to each patient's individual needs.
  3. Critical Care Services: Anaesthesiologists play a crucial role in the management of critically ill patients in intensive care units (ICUs). They are skilled in airway management, mechanical ventilation, hemodynamic monitoring, and resuscitation techniques, providing essential support for patients with life-threatening conditions. Anaesthesiologists coordinate multidisciplinary care teams, assess patients' clinical status, interpret diagnostic tests, and make critical decisions regarding treatment and interventions in the ICU setting. They also contribute expertise in perioperative care for patients undergoing high-risk surgeries or those with complex medical conditions.
  4. Perioperative Medicine: Anaesthesiologists are involved in perioperative medicine, which focuses on the care of surgical patients before, during, and after surgery. They optimize patients' medical conditions, manage comorbidities, and reduce surgical risks through preoperative assessment and optimization clinics. Anaesthesiologists collaborate with surgeons, internists, and other specialists to develop personalized care plans, minimize perioperative complications, and expedite postoperative recovery.
  5. Education and Research: Anaesthesiologists are educators and researchers who contribute to the advancement of medical knowledge and the training of future healthcare professionals. They participate in medical education programs, residency training, and continuing medical education activities to teach and mentor students, residents, and fellows. Anaesthesiologists also conduct clinical research and quality improvement projects to improve patient outcomes, enhance safety practices, and innovate new techniques in anesthesia, pain management, and critical care.
Overall, anaesthesiologists play diverse and essential roles in anesthesia administration, pain management, critical care services, perioperative medicine, education, and research. Their expertise and contributions are integral to ensuring optimal patient care across a broad spectrum of medical specialties and healthcare settings.
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It's important to note that the decision to initiate ECMO therapy is made on a case-by-case basis, considering factors such as the severity of illness, the potential for recovery, and the resources available. A multidisciplinary team, including critical care physicians, ECMO specialists, and respiratory therapists, typically evaluates each patient to determine the appropriateness of ECMO therapy.
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The indications for initiating ECMO therapy in patients with respiratory failure:
  1. Severe Acute Respiratory Distress Syndrome (ARDS): ECMO may be considered in patients with ARDS who have refractory hypoxemia (low blood oxygen levels) despite optimal mechanical ventilation.
  2. Failure of Mechanical Ventilation: Patients who fail to respond adequately to conventional mechanical ventilation, including high levels of positive end-expiratory pressure (PEEP) and prone positioning.
  3. Hypercapnic Respiratory Failure: In certain cases of severe hypercapnic respiratory failure, especially in patients with obstructive lung disease like severe asthma or chronic obstructive pulmonary disease (COPD), ECMO can provide respiratory support while allowing for lung protective ventilation.
  4. Bridge to Lung Transplant.
  5. Intractable Respiratory Failure: Due to conditions such as pneumonia, pulmonary embolism, or acute exacerbations of chronic lung diseases, ECMO may be considered when conventional therapies are ineffective.
  6. Acute Respiratory Failure in Immunocompromised Patients: ECMO may be considered in patients with severe acute respiratory failure, such as those with hematologic malignancies or following hematopoietic stem cell transplantation, who have a reversible cause of respiratory failure.
It's important to note that the decision to initiate ECMO therapy is made on a case-by-case basis, considering factors such as the severity of illness, the potential for recovery, and the resources available. A multidisciplinary team, including critical care physicians, ECMO specialists, and respiratory therapists, typically evaluates each patient to determine the appropriateness of ECMO therapy.
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Epidemiology of infectious diseases
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Some of the key challenges gathered:
1. Infection Control: Infectious diseases can be highly contagious, and strict infection control measures are crucial to prevent the spread of the disease among patients, healthcare workers, and the broader community. Critical care and anesthesia units need to have robust infection controlprotocols in place, including appropriate isolation procedures, personal protective equipment (PPE) usage, and disinfection practices. Balancing the need for effective infection control with the provision of necessary care can be challenging.
2. Transmission Risk: Healthcare workers, including critical care and anesthesia providers, are at an increased risk of exposure to infectious diseases due to close contact with infected patients, aerosol-generating procedures, and potential exposure to bodily fluids. Adequate training, adherence to infection control protocols, and availability of appropriate PPE are essential to minimize the risk of transmission to healthcare professionals.
3. Resource Allocation: Infectious disease outbreaks can strain healthcare resources, including critical care beds, ventilators, medications, and specialized equipment. The increased demand for these resources during outbreaks may require careful allocation and prioritization of resources to ensure optimal care for critically ill patients. Ethical considerations, such as fair distribution and maximizing the overall benefit, may come into play when making resource allocation decisions.
4. Diagnostic Challenges: Prompt and accurate diagnosis of infectious diseases is crucial for appropriate patient management. However, some infectious diseases may present with nonspecific symptoms or have overlapping clinical features, making diagnosis challenging. Access to rapid and reliable diagnostic tests is essential to facilitate timely and accurate diagnosis, which can impact treatment decisions and infection control measures.
5. Staffing and Workforce Management: Infectious disease outbreaks can lead to increased patient loads and workforce demands, potentially straining the healthcare system. Adequate staffing levels, including trained critical care and anesthesia providers, are essential to meet the increased demand for services without compromising patient care. Ensuring the physical and mental well-being of healthcare providers is crucial to sustain the workforce during challenging times.
6. Evolving Knowledge and Guidelines: Infectious diseases often present new challenges and require healthcare providers to stay updated on the latest knowledge, guidelines, and best practices. Rapidly evolving evidence and changing recommendations can pose challenges in providing consistent and evidence-based care. Continuous education and training are essential to ensure healthcare providers are equipped with the most current information and can adapt their practices accordingly.
These challenges highlight the importance of preparedness, infection control measures, collaboration across healthcare teams, and ongoing education and training to effectively provide critical care and anesthesia services in the context of infectious diseases.
Hope it helps
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How many days Arctic sun can be used to maintain temperature?
Head injury protocol can be disconnected abruptly? If not, what criteria can be used to taper and disconnect the protocol.
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Monitor GCS
If ICP < 20.
Brain oxygen > 20
GCS is proportional to cerebral oxygen ation
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Hi everyone,
ICU nursing staffing's impact on patient (and other) outcomes is well documented in the literature. Nonetheless, methods (e.g. Nursing activities score) have been criticized during the last decade for not including several aspects of the nurse's work besides bedside duties.
Currently, which would be the most valid approach /tool to objectively estimate nursing staffing?
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The NAS is being referred to in terms of workload in the ICU. Please read the article below
DOI: 10.1016/j.iccn.2018.06.005.
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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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Is it a routine in your intensive care unit to perform ultrasound-guided central venous catheterization?
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I am responding to this question 6 years later.
The cebtre i work, in Sri Lanka, we routinely use ultrasound during central line placements.
Majority are Internal jugular lines.
Only when the Ultrasound is occupied elsewhere, we go for land mark guided technique.
Practically,subclavian line insertions under Uss guidance is bit difficult, but for that too, the USS is of great help and improves safety profile....
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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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Which methods does they suggest to ease the burden and stress as a teamwork?
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I would like to assume that frontline workers dealing with the COVID - 19 pandemic would have been given access to mental health resources. However, it not there are several ways this can be achieved - (e.g., individual vs group basis). It might make sense to begin forming a group (lead by a mental health professional) where workers can share stories with one another. This would help provide an "outlet" for those needing one, as well as hear how others are coping, which they may find helpful. In addition to providing support, this group can also help identify individuals who would need more intensive therapy/counseling that can be provided individually.
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My above publications are already published on line at bsccmjournal.org and at banglajol.info/index.php/BCCJ
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How to add research is well described topic at RG Help Center page:
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Apparently bacterial superinfection translates into worse outcome when a patient is tested positive with SARS-CoV-2 and has developed symptoms. This is especially worrisome as the acquisition of any bacterial superinfection seems to be of higher likeliness in critical ill patients according to the few studies addressing the matter so far. Even more so, when we learn, that patients had acquired a bacterial superinfection despite being prescribed antibiotic prophylaxis with the onset of symptoms! We can also learn from actual data, that bacterial superinfections, occurring under prescription of empiric antibiotic medication, had a higher association with fatal outcome. The findings suggest, that patients had acquired or were colonized with a multi-resistant strain during or even prior to their hospital stay. In current publications addressing the matter, however we learn that only about 30% of the strains where resistant to the antimicrobial therapy administered. We therefore must take into consideration that there is a lack of accumulation of MIC of the antimicrobial in the respective tissue during the course of the illness in the 70% of patients, that had acquired a bacterial superinfection with normal susceptibility of the pathogen to the prescribed antimicrobial. This very scenario is held accountable for the development of resistance mechanisms in endemic pathogens. This might display a potential explanation for the selection of multi-resistant pathogens in the course of SARS-CoV-1. However, the course of SARS-CoV-1 was well controllable at that time. We are facing a different scenario in this ongoing pandemic. Whereas IFR and CFR in COVID-19 remain single digit, the wide use of empiric antibiotic prophylaxis might shift morbidity and mortality by promoting bacterial resistance to other dimensions for all of us in the long run.
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I think there is a misunderstanding, and there is no evidence to my knowledge, that antibiotics might bear the risk of inducing sensitivity or causing shortness of breath in COVID 19. There is general evidence for adverse effects in certain patients for some antibiotics, but this is not limited to COVID-19 patients, at least to my knowledge.
This discussion's results, so far:
  • Inappropriate use of antibiotics is taking place, because of a large expansion in the number of patients with respiratory tract symptoms due to COVID or not, worldwide.
  • The more any bacteria are exposed to antibiotics through treatments that are unnecessary, the higher is the chance to develop resistance.
Bottom line:
  • antibiotics should not be prescribed unless there's a clear indication
  • Pathogen retrieval should be conducted to give guidance in antibiotic treatment of any suspected bacterial superinfection in COVID-19
  • no clear denominator for empirical use of antibiotics in respiratory tract infections due toor associated with COVID-19
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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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Excess deaths occur when the capacity to deliver critical care to patients with Covid-19 is exceeded (i.e. those who require organ support do not receive it). This is happening around the world now. The media has sensationalised discussions on numbers of ventilators and the availability of ICU beds. Unfortunately, the capacity to deliver healthcare is in fact most limited by human resources. Furthermore those healthcare professionals on the frontline are at greatest risk of contracting the virus.
To improve patient outcomes during the ongoing Covid-19 pandemic; the capacity of healthcare systems to prevent, detect and treat acute respiratory illnesses must be increased. This requires an increase in the number of staff who can do this. The fundamental question is: how can this be achieved now?
Online educational materials have been developed to train healthcare professionals in the basic principles of intensive care. However, this does not help people at the bedside faced with a crashing patient. I believe that familiarisation of staff with the use of systematic checklist proformas for the assessment of critically ill patients (see review above) can increase the capacity of healthcare systems to deliver critical care.
Does anyone have any other ideas? Please share them.
Thank you.
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As per Indian a context, there is enough scope to train medical staff to meet the shortfalls. There are almost surplus staff of dental sciences graduate and technician's. These wel educated medical professionals already having enough trainings and can be further improved by short-term trainings. Similarly, other countries can adopt such individual's to serve covid19 pandemic.
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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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53 Y Female was exposed to boiled water which fall on her abdomen. She left the burn untreated and scab formation occurred. TBSA expected 1-4% , probably superficial partial thickness burn. How would you manage this burn? Peel the scab and create a moist wound environment? Or what procedures would you follow now after the scab has formed?
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You would need to determine the depth of the burn and predict healing potential: whether it will heal spontaneously or would need excision and grafting. If grossly infected the wound needs to be debrided early. If not the wound could be dressed with silver sulfadiazine for a few more days to see if the "scab" separates off which would allow you to reassess better.
If you still would have a layer of ?eschar after a week the burn wound is most likely deep and would need excision and grafting.
Posting a picture would help a lot.
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I am looking for an author to write a chapter for a book I am editing. The chapter is about ethnographic research into critical care. Are you interested in writing this chapter or do you know someone who may be interested?
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Revered Professor Paul M.W.Hackett,
I am happy to have known that you are writing a Book on Ethnography. I am teaching Ethnography Field Research for Rural Development more than a decade in the Department of Rural Development and Agricultural Extension, College of Agriculture, Wolaita Sodo University, Ethiopia, East Africa. I will be grateful to you Prof if I will have an opportunity to help you. I would like to know information from you Prof. I went along with my M.Sc. students to have Ethnography Field Survey on Australia funded Carbon Project near to my WSU university.
Regards
M.Senapathy
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I'm looking for some inspiration around methods for measuring usability of a bedside testing device in critical care. Any tools and ideas would be great.
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Lewis, why are you bringing up these devices without knowing anything about what the device is they are evaluating? She is asking about the methods for usability evaluation.
Natalie, look at some of the literature regarding Human Factors at
Also some recognized standards such as IEC 62366.
There are also some dedicated service providers with expertise in usability engineering standards that might have free white papers.
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Here is a question for everyone that I am currently stumped on:
Is there some standardized metrics or quality targets for in-hospital cardiac arrests rates?
Its related to the work I am doing to implement CCOT at SPH. The CCOT literature uses a variety of measures and it gets a little confusing:
· Code blue (all types) per 1000 admissions or per 1000 discharges
· Cardiac Arrest (only code blue with CPR) per 1000 admissions or per 1000 discharges
· Code blue or Cardiac arrest excluding critical care areas (i.e., ED, ICU, CCU, CSICU, OR/PACU) per 1000 admissions or discharges
I looked through CIHI and it does not look like they have any stats on in-hospital cardiac arrest rates that I could find. We keep track of code blue data, but I don’t think it is reported to any external organizations. The UK and Australia have done rapid response systems for far longer, but I haven’t come across any official standardized metrics or definitions of what is considered good, bad or ugly in the way of targets.
Thoughts?
Thanks in advance for any assistance you can offer.
Vini
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I agree with Nikola Bradic
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I am begin work on a doctoral project related to nursing perceptions of critical care nutrition and attempting to identify the theoretical framework I will use to guide my study. I am currently leaning towards the health belief model, but am open to other ideas and suggestions.
Thank you.
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To assure good practice, theories, fundamentally, are formulated to describe, forecast, and understand phenomena. The theoretical framework presents and indicates the theory that elucidates why the research problem under study exists. It is also the structure that can hold or support a theory of a research study
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What can we do to make our students more careful when it comes to basic and core subjects in Nursing? What can we do to enrich students' experience in the clinical settings to become more conducive and achieve the learning objectives? What can we do to make our students become more sensitive to patient needs, the implicit as well explicit ones?
Dear Colleagues
I would like to share with my experience and see whether you similar or different experiences. Firstly, I have a very strong clinical orientation, especially in different critical care units. I still entertain myself with nurses at the clinical setting by asking and working with patients during my work day as a course coordinator to the clinical courses. I have many issues with the opportunities provided to our students to learn by observing and by participating, under guidance, in the process of caring for patients. Often, I experience very disappointing moments in my life, I rarely experience somewhere else, when I ask students about very simple, basic knowledge of anatomy, physiology, pathophysiology, and pharmacology. Students do not have answers. I know for sure these topics have been elaborately explained to them by either me or my colleagues, in this this course or in that. But the result is usually the same; Sir, these topics have not been explained to us, you know". Well, indeed, I know that they were not honest, or perhaps they forgot. Hope to get some response.
Cheers, Lourance
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Today, considering the change in learning needs, changes of the pattern of diseases, and increased care needs, on the one hand, and the shortage of nurses as the largest part of the healthcare team as well as very high cost in nursing and medical education, on the other, the importance of caring for proper clinical education has been multiplied
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A large number of studies have reported that MEWS is an effective tool for predicting in-hospital mortality. However, there are variations in cut-off point (for mortality prediction). There are studies that consider MEWS ≥ 6, others that mention MEWS ≥ 4 as a risk factor for mortality. What cut-off value do you consider?
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7-8 consider in-patient treatment
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Beyond the events on October 16th, 1846 ("Ether Day"), which stories are worth to be recognised about the history of Anesthesiology? Which are the most impressive, curious, or funny things we should remember?
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These anecdotes are fun reading, but if you really want to learn how real medical science advanced, and how modern anesthesia evolved during the prelude to WWI, you should read Crile's book "Anoci-Anesthesia" that is available free on the Internet. It is a classic. Crile was a master surgeon and serious researcher who built his own dog laboratory and methodically studied pathophysiology. You should also read the screeds of Ralph Waters, the founder of MD anesthesiology, and the publications of Yandell Henderson, who proved the clinical benefits of CO2.
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In your point of view, which are the most important points we should discuss concerning intubation / airway management in trauma patients with unstable c-spine fracture?
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Airway management in unstable cervical spine fracture patient is always challenging. The primary reason for intubation may differ in different situations.It can be both difficult as well as dangerous due to various factors and always needs to be individualised with minimised spine movements.
Patient related factors-
Urgency of intubation- can be immediate, emergent, urgent or elective- actually dictates the decision, technique of airway management as well as drug used. The patient may be hypoxic, almost in arrest to relatively stable.
Level of injury (e.g. C1-C2 or lower cervical), Degree of instability and Severity of spinal cord compression, Anterior or posterior compression (which movement can aggravate the compression and hence to avoid), Presence of Spinal shock, Immobilisation
Presence of traumatic brain injury (increased ICP) and/ or polytrauma leading to shock or crush injury (dose and response to drugs) Facial or airway trauma, Full stomach status, Anatomical factors for difficult airway.
Other factors to be considered-
Level of experience of the person performing intubation
Equipments available for intubation (special equipments- videolaryngoscopes or flexible scopes), Drugs available for intubation, Time and place of intubation (ER/ Trauma ICU/ primary care center before transfer).
Later on, presence/absence of major neurological deficit also affects technique of airway management though such assessment may not be possible in emergent unconscious patients.
Additionally, often the issue is whether to intubate (in inadequately equipped place by inexperienced person) and then transfer to higher center is safer or the other way round. Mode of transport also needs to be addressed.
It must be appreciated that airway management is not just a technique bur a sequence of pharmacological and technical interventions right from suction and oxygenation done in least detrimental way.
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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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Is anyone in monitoring of oximetry tissue  Rigional except pulse oximetry
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We routinely use INVOS for monitoring during surgical carotid endarterectomy,and are extending it into monitoring during stenting and other invasive interventional procedures.
Simple to set up and use,pretty resistant to forms of interference such as movement and electrical noise.
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My topics and questions are only in the early stages and haphazard. It will be a literature review. So far I am thinking of the effects of sedation breaks in adult ICU patients. Early mobilisation, the psychology effects on long term ICU patients, Are the medical profession overdosing patients who are sedated with opioids/ maybe over use of opioids in the sedated patients. Trying to get an idea of where to go what topic Il get the most information on and develop a question.
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Nikola Bradic, I like the dexmedetomidine although I believe that remifentanil is actually a poor choice:
1. Cost (most expensive choice in the US)
2. Higher adverse reactions
3. Tolerance quicker
4. Hyperalgesia more common in remi.
If study is planned... a new intervention compared to usual care is a better choice. There is the option for a three group study.
IMHO, warmest regards,
Christopher
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I am conducting a study evaluating risk for pressure injuries among critical care patients. I have EHR data pertaining to moisture, nursing skin assessments, body temperature, and also medical devices for surgical critical care patients. I would like to find a way to indirectly assess micro-climate.
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Dear Jenny
I'm studying skin microclimate in Brazil and the relationship with the pressure injuries development.
You may send me a private message.
KR
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I was wondering if any of you are aware of any sepsis pertinent severity score, not APCHE or SOFA?
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Thanks.
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Inflammatory mediators promote insulin resistance, suggesting perhaps that critical care patients may exhibit hyperinsulinemia. However, I have great difficulty finding an article referring to serum insulin levels (there is an overabundance of publications on hyperglycaemia and insulin resistance but not insulin).
I would very much appreciate it if anyone can refer me to a manuscript making reference on insulin levels in any severe inflammatory setting (burns, sepsis, trauma, and surgery… any context where a strong inflammatory response is solicited).
Note: hyperglycaemia is often treated with intensive insulin therapy –it would be super if the study refer to untreated patients.
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Hi Ian, many thanks!
Honestly, I was absolutely smitten as why I could not find any reference to serum insulin levels. However, that there is in fact not many publications on this topic is even stranger though...
In any case, articles definitely seem relevant. Will most certainly have a closer look -thanks!
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Dear colleagues,
Health professionals face difficult decisions in emergency medicine and trauma and critical care and deal with uncertainty. Sophisticated decision making tools could help reduce uncertainty and doubt and speed up decision making.
Would a decision assisting tool be helpful in EM and Critical Care, that based on "big data"  predicts potential diagnoses, outcomes and events and makes management suggestions to the team ?
What are your thoughts?
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Any of the studies that have developed decision tools in these two arenas of medicine are based on guidelines formulated from large samples of data.  Thus the information from these guidelines are only that--guidelines that are based on a central tendency finding in the data.  In practice, however, the treatment as well as the clinical pathway needs to be tailored to the specifics of that individual patient and that patient may not "fit" within the guidelines of that central tendency.  The art of medicine is based on the individual needs of that patient.
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Risk factors for CRBSI are well documented but I´m looking for a sort of screening tool in ICU pacientes with CVC.
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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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vaECMO in cardiogenic shock results in competing flows (ECMO vs. heart) and can impose increased afterload on the left ventricle. How can hazardous elevation of LA-pressures be anticipated and handled under peripheral vaECMO.
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does anyone see severe hemolysis associated with pulmonary vein drainage for LV venting?
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I am looking for any research comparing patient-focused outcomes between ALS-level care and prehospital critical care for OHCA.
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Many thanks for your help and suggestions everyone!
I have included pubmed and google scholar in my research strategy, amongst others. I  also decided to use twitter and researchgate to look for grey literature, which might not be identified by the traditional searches. I managed to find one additional publication through this, so all good.
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I want a tool to measure communication difficulty for a ventilated patient
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 thank you all.
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Do you have any publications/books where I can find the information about duration of a single respiratory rehabilitation intervention on a mechanically ventilated patient in Intensive Care Unit? 
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It will depend on specific objectives you aim and for how long the patient remained intubated. I think that for a safe extubation more tham a single respiratory rehabilitation will be needed and for more median of 2 to 4 weeks of muscle training. But I agree that there is a lack of evidence, mainly because these situations are too much variable (time of intubation, clinical condition and performance status of the patient, team skills,  etc).
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What is the real risk of cardiac tamponade?
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Tunnelled central catheter tips should, in my opinion, be sited just inside the right atrium.  This eliminates the risk of SVC stenosis and fibrin sheath formation - both of which are major problems in dialysis patients and those dependent on long-term TPN etc. Although I have no data to show that my 25 year experience has not led to atrial arrhythmias, I concur with the observation above that ventricular, rather than atrial arrhythmias are observed when guidewires are introduced.  These are invariably benign and self-limiting in my experience and to do with wire movement. 
Hickman's original paper title says it all: Surg Gynecol Obstet. 1979 Jun;148(6):871-5.
A modified right atrial catheter for access to the venous system in marrow transplant recipients.
Hickman RO, Buckner CD, Clift RA, Sanders JE, Stewart P, Thomas ED.
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Intraoperative awareness may lead to catastrophic psychologic sequelae (1), a fact motibating anesthesiologists to use neuromonitoring in oder to prevent awareness during operation. In the "B-Aware" trial, awareness associated with a BIS-guided protocol in patients at high risk of awareness occurred substantially less frequently than did awareness events in the control group (2). However, neuromonitoring on the basis of the bispectral index (BIS)-monitoring is mostly used for anesthesia induced by propofol and evidence for the safe prevention of awareness in patients monitored with BIS during narcosis induced by volatile anesthetics is limited.
1. Lennmarken C, Sydsjo G: Psychological consequences of awareness and their treatment. Best Pract Res Clin Anaesthesiol 2007; 21:357– 67
2. Myles PS, Leslie K, McNeil J, Forbes A, Chan MT: Bispectral index monitoring to prevent awareness during anaesthesia: The B-Aware randomised controlled trial. Lancet 2004; 363: 1757– 63
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Dear Dr. Castellanos, thank you for your thoughts. It is indeed of great importance to get immediate feedback from our surgical colleagues so the neurophysiological condition can be estimated more precisely. I also agree with Dr. Felsby that muscle twitching in non-relaxated or insufficiently relaxated patients shoul not be misinterpreted as awareness. If muscle activity alone is over interpreted as awareness, the patient is at great risk of being anesthezied too deeply.
On the other hand, I agree with Dr. Castellanos that conversations held during an operation should never be directed towards a direction that could be discomforting the patient, as all our measures aiming to detect awareness are unsafe and providing limited information regarding the neurophysiological and neurocognitive states of our patients. I therefore recommend close clinical observation and additional interpretation of the electroencephalogram (EEG) (although only frontal EEG  traces are available from routine bispectral index (BIS) monitoring) in addition to the monitoring of the numerical BIS, end-tidal concentrations of the volatile anesthetics and the variability of vital sings. However, there are no data regarding the safety of such multimodal monitoring regarding the prevention of awareness and studies in this context are urgently needed.
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The image becomes visible after opening the question. The ensuing discussion provides the interesting bottleneck of this problem though. Any help would be much appreciated.
PS. the last sentence on the image is irrelevant and should have been cropped. 
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Dear Dr van Jole:
1-Primary Haemostasis
It is the set of events that leads to platelet plug formation, first step in stopping the bleeding, preventing release of cellular components of blood. During this phase involves two mechanisms: a vascular and other platelet.
• a) vascular spasm. Immediately to the production vessel rupture way, a powerful contraction of muscle fibers of the same occurs. The result is a decreasing vasoconstriction vessel diameter, and even if it is small can reach close, reducing blood loss.
• b) Formation of platelet plug. In the formation of the platelet plug can distinguish the following steps:
1. Accession or platelet adhesion.
2. secretion and platelet aggregation.
1-Accession or platelet adhesion
After the rupture of the vascular endothelium platelets adhere to subendothelial structures, mainly collagen fibers that arise by broken surface will contact and platelets. In this process platelets lose their discoid shape, becoming spherical and emitting spikes through which adhere to surrounding tissue. In the process of joining various platelet membrane glycoproteins are required, the plasma von Willebrand factor and subendothelial collagen and basement membrane. This process lasts very little, about 2-3 seconds.
Normally, the endothelium functions as an inert surface for hemostatic factors that circulate within the vessel. Any change in the endothelial wall, can lead to activation of coagulation and their regulatory systems. Vascular injury can occur directly or indirectly. Initially, when the vascular endothelium is damaged, it responds with a local vasoconstriction induced by platelet released serotonin. The exposure of the underlying collagen fibers subendotelio attract the circulating platelets adhere to collagen trying to close the endothelial defect and experiencing significant metabolic changes that promote continuity of hemostasis.
2-secretion and platelet aggregation
It is called the aggregation process by which platelets are fixed to each other. This process requires Ca ++ and ADP to be released from platelet granules by a process called platelet activation or secretion.
Platelets undergo a profound structural transformation. Membranes dense granules bind with the plasma membrane, releasing their contents to the outside and α granules release their contents. The released substances have very different types of biological activity:
• Stimulate changes estrucuturales own platelets.
• Increase in platelet adhesion and platelet granule secretion more.
• Increase the recruitment and activation of additional platelets.
• favor the aggregation and coagulation.
• Platelets possess on its surface adhesion molecules belonging to integrin family, which serve as receptors for various substances involved in platelet adhesion and aggregation, such as von Willebrand factor (vWF) and fibrinogen (FIB). Either by their adhesion to collagen, in contact with thrombin (TB), or by the action of platelet activating factor (PAF) produced by monocytes / macrophages (MON / MF) and polymorphonuclear (PMN); platelet activating your metabolism producing ADP, serotonin and Ca ++ dense granules, and other pro and anticoagulant substance of their alpha granules. Alongside the path of Phospholipase A2 (FA2) which releases arachidonic acid (ACA) is activated. This AcA, is metabolized by cyclooxygenase resulting in a series of cyclic endoperoxides that form in the endothelium Prostacyclin (PGI) of antiplatelet effect; and platelets by the action of thromboxane synthetase will result in thromboxane A2 (TXA2), potent platelet aggregating local and vasoconstrictor. AcA share equally the lipoxygenase metabolites produced family of leukotrienes, which are activators of PMN and MF .In this activation process, platelets change their discoid shape to a spherical structure with internal extension and contraction pseudopodia his cotráctil actin-myosin system, after the release of Ca ++ and generation of prostaglandins (PG). Thus they served on platelet thrombus.
That is, stimulated platelets in their adherence to subendotelio, TB and PAF, free Ca ++ activates the system actin-myosin coupling. TXA 2 mobilizes and involves other circulating platelets; and these reactions release the contents of dense granules - secreción- initiating similar phenomena in the surrounding chain platelets. Later receivers exposed for FIB and platelet aggregation begin to form the thrombus. This primary plug must be stabilized by fibrin deposition, final product of the coagulation cascades that form the plasma phase
   
This discharge produces more changes in platelets adhered and attracts other platelets, gradually adding to leave. Platelets are held together by bridges link between their membranes and subendothelial tissue. Thus a barrier is established, yet permeable for the free spaces left between platelets, but forming an initial line of defense, platelet plug or thrombus blank for the subsequent performance of the process of coagulation.
3 - Secondary haemostasis or coagulation
It is a process that modifies the liquid state of the blood giving it a gel structure type. It is the transformation of a soluble protein, fibrinogen, into an insoluble protein: fibrin; forming a mesh or net enclosing formed elements (clot), thereby strengthening the bond between platelets in order to permanently prevent bleeding.
Schematically it can be represented as an enzymatic cascade by and plasma proteins.
It has several phases:
1. Formation of prothrombinase or prothrombin activator.
2. Formation of thrombin.
3. Formation of fibrin.
This plasma coagulation phase begins with the activation of the contact system factors: Factor XII (FXII), XI (FXI), IX (FIX). Prekallikrein (PK) and high molecular weight kininogen (HMWK), the latter resulting kallikrein (KK) and kinin (K) respectively. All of these factors are the intrinsic coagulation pathway, because its components are in the plasma. The extrinsic pathway begins with the expression of tissue factor (TF) which activates factor VII (FVII). Both routes lead to the common pathway with activation of factor X (FX) in the presence of Factor V and prothrombin transform Ca ++ (PTB) in TB, and this in turn IFF fibrin monomers and fibrinopeptide A and B. the factor XIII (FXIII), activated TB and FXII, stabilizes the soluble fibrin monomers in polymers and insoluble stable serine protease coagulation are activated with the help of cofactors - FV, Ca ++ and factor VIII by both tract, for cascade mechanism whose final product is the fibrin network, which together with platelets form the final haemostatic .Paralelamente to serine protease members coagulation pathways, a series of inhibitory proteins coagulation try to maintain a stable equilibrium, the final product is the blood flow and maintaining circulation. Thus, for the extrinsic pathway inhibitor of tissue factor (ftpi) produced in the endothelium, that seek to regulate this pathway is known. Endothelium also produce thrombomodulin (TRM), responsible for modulating the action of TB, which activates protein C (PC) which together with its cofactor Protein S (PS), exert anticoagulant and fibrinolytic action. Also described is an endothelial inhibitor PC (IPC) that regulate this anticoagulant mechanism.
   
3-1 prothrombinase Formation
You can follow two paths:
• extrinsic extravascular or exogenous pathway (see diagrams of the presentation in supplementary material).
• Intrinsic, intravascular or endogenous pathway (see diagrams of the presentation supplemental material).
The two-way match for activating the X factor from this point form the final common pathway. This factor along with platelet factor 3, calcium and factor V form an enzyme complex called prothrombinase and prothrombin activator.
3-2 Formation of thrombin
It is performed in a single reaction of prothrombin (Factor II).
3-3 in blood is present an inactive protein, Factor I or fibrinogen.
Thrombin catalyzes the splitting of this molecule to form fibrin monomers, soluble and unstable in the presence of Ca ++ and Factor XIII are polymerized activated; forming an insoluble polymer in the form of three-dimensional mesh network or closes the spaces between the platelets and seals definitively the platelet plug, resulting in the red thrombus or clot
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Can any intensivist in Europe who has adopted CoBaTriCe program explain to me how trainees are evaluated and who are the evaluators?
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Hi Andrea. I can tell you how Emergency Medicine trainees are assessed .
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What this articles addresses, e.g., the differential diagnosis of CAPS, is something I brought up a long time ago, especially at the Galveston APS meeting a few years ago. In this regard, when talking about the longstanding CAPS registry, how do we know if all those patients actually had CAPS versus some of the other entities, e.g., HU syndrome, TTP, underlying infections, malignancies, HIT, etc? Antiphospholipid antibodies have been reported in the presence of infection, and I can easily imagine a patient in a critical care unit developing septic shock with positive antiphospholipid antibodies, not necessarily having CAPS in this setting.
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This is quite debated and confusing to detect living CAPS. According to the citeria of APS, either LA and/or aCL and/or B2GP1 should be present (12 week apart 2 positive results). Clinically the patient should present thrombotic events (stroke, myocardial infarction, gangrene, pulmonary embolism or DVT) or recurrent miscarriages. However in case of CAPS, kidney and liver function might be disturbed. The major cause of CAPS death is multiple organ failure. APTT might be consistantly significantly high even after regulated warfarin dosages. Please share your experiences as well as this question was posted 1 year back. 
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Atropine is of no use to stimulate breathing in cholinergic crisis, and mechanical ventilation is the only option. What potential therapeutic agents can be designed to reverse this phase in critical care practice? 
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Dear Rafik,
Thanks for your reply. Yes this is an interesting topic since this topic involves intriguing interplay between ACh, muscarinic, and nicotinic receptor actions.
Atropine as we know is a competitive antagonist of ACh at the muscarinic receptors. The muscles of respiration are innervated by cholinergic nicotinic receptors, so atropine is of no use in this sense. 
 Almost all anticholinesterase agents or cholinesterase inhibitors are contraindicated in cholinergic crisis; distigmine is not an anticholinergic agent rather it is a cholinomimetic drug similar to neostigmine or physostigmine. There's no rational for using muscarinic agonists as well, since most of these agents are cholinomimetic / parasympathomimetic, and dangerous if used in acute respiratory failure due to cholinergic crisis (often on account of organophosphate poisoning [OP]) or due to over-treatment of myasthenia gravis with distigmine (AChI toxicity). One option which could be explored: if any targeted nicotinic receptor analogue which would selectively bind to ACh nicotinic receptors on the diaphragmatic muscles may be of some use. You have very little choice for drug therapeutics in the way of giving anticholinergic agents (atropine, or pralidoxime which is effective only in OP) or experimenting with drugs that block the synthesis of ACh, but this would likely, in any case of MG, would further worsen the symptoms. Transient inhibition of the enzyme choline acetyltransferase would result in motor neuron dysfunctions, so this is not an option as well. Drugs like kainite, or hemicholine which block the reuptake of choline may reduce synthesis of ACh, so may act as an indirect acting anticholinergic agent. But it has got no clinical use.
Regards, Sidharta
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Recently this article was published in Critical Care:
It included risk factors for VTE specific for ICU patients (such as sedation and vasopressors). table 3
My question, if we are to include these risk factors in a VTE risk assessment score, how many points each should be accounted for?
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Absolutely correct, Vishnu Mani. Thank you.
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There are some exclusions from ICU mortality rate, like the age, burn cases, etc.
Are there any others? Please provide a link to evidence.
When I calculate crude mortality rate in ICU the formula is:
total deaths / total discharges in the same period, but some exclude ( as far as I know ) DNAR cases from the numerator, are there any other exclusions.
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Dear Yalim Dikmen, thank you very much, I agree that this is a better measure, and I suggested that to my board, but till now the official measure is crude mortality.
Thank you
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Are there any Critical Care documents EWS, Evaluation and Daily entry charts available in the public domain for use in Africa
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The NEWS is available for adult inpatients in the UK - on RCP website seehttps://www.rcplondon.ac.uk/resources/national-early-warning-score-news 
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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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My experience is that APPs can provide quality care to the majority of critically ill patients.  By incorporating Physician Assistants (PA) and Nurse Practitioners (NP) with telemedicine capabilities, I feel critical care can be greatly improved in smaller, rural hospitals.
Thoughts?
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The observations needed to answer this question is the evidence of PA/NPs in ICUs.  In this regard there are at least 10 good (and 2 very good) studies that shows the care/outcome is equivalent to MDs.  So the subsitution factor is in place.  The other is the role in rural health.  If we use the NCHS definition of most rurality and look at those providers occupying rural and critical access hospitals and territorial hospitals (~1100) we see an increasing presence of PA/NPs and a decreasing presence of MD/DO/MBBSs.  No one should deny that an MD is ideal in these situations but if need outstrips desire than employing PA/NPs in these critical roles may be the next best thing - all things considered.  Research on this matter is in short supply.  
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I Work with trauma patients. If anyone knows specific material for such patients you helps even more. Thanks in advanced. 
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Dear G.D. Ceniccola,
maybe you can use the following information…
Coltman A, Peterson S, Roehl K, Roosevelt H, Sowa D. Use of 3 tools to assess nutrition risk in the intensive care unit. JPEN J Parenter Enteral Nutr. 2015;39(1):28-33. http://www.sifoweb.it/images/pdf/attivita/attivita-scientifica/aree_scientifiche/nutrizione_clinica/letteratura_internaz/Use_of_3_Tools_to_Assess_Nutrition_Risk_in_the_ICU.pdf
Heo GJ, Kim HJ, Hong JI. Comparison of nursing records and the catholic medical center nutritional risk screening as a nutrition screening tool for intensive care unit patients. Clin Nutr Res. 2015;4(1):56-62. http://e-cnr.org/Synapse/Data/PDFData/9994CNR/cnr-4-56.pdf
Aitken K, Cummins P, McDougall M. Inter-rater reliability of the fife intensive care unit nutritional screening tool: http://www.scottishintensivecare.org.uk/uploads/2014-05-28-22-01-12-nutritionalscreeningpdf-54540.pdf
Lomivorotov VV, Efremov SM, Boboshko VA, Nikolaev DA, Vedernikov PE, Deryagin MN, Lomivorotov VN, Karaskov AM. Prognostic value of nutritional screening tools for patients scheduled for cardiac surgery. Interact Cardiovasc Thorac Surg. 2013;16(5):612-8. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3630415/pdf/ivs549.pdf
Lomivorotov VV, Efremov SM, Boboshko VA, Nikolaev DA, Vedernikov PE, Lomivorotov VN, Karaskov AM.Evaluation of nutritional screening tools for patients scheduled for cardiac surgery. Nutrition. 2013;29(2):436-42. https://www.researchgate.net/publication/233826629_Evaluation_of_nutritional_screening_tools_for_patients_scheduled_for_cardiac_surgery
Hodges BM, et al. Nutrition management in the intensive care unit. Pharmacotherapy Self-Assessment Program, 5th Edition; p 141-57. https://www.accp.com/docs/bookstore/psap/p5b7sample03.pdf
Best wishes from Germany
Martin
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What is the best option: human fibrinogen or cryoprecipitate?
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Yes, we analyse the coagulation profile with thrombelastograpy and if we have hypofibrinogenemia, we use haemocompletan, 1 g /botle 
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In relation to critical care.
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In my opinion, "passive leg raising (PLR)" test would be most valuable and easiest measurement of fluid responsiveness. Echocardiography is also useful device, but, it is needed to experienced clinicians and it is quite expensive. Pulse pressure variation might be helpful in intubated patients, but i think spontaneous breathing or arrhythmic patients, PLR would be the best.  
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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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It is very interesting which vein is the most popular in your institution.
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all central venous access, but mainly subclavian route
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I utilize Gambro Prismaflex system - Prismocitrate 18/0 (CVVHDF).
Could you be so kind as to send me such a protocol?
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Hello Tomasz. I have attached our CRRT guidelines from the Vanderbilt Children's Hospital. We have used this with great success. Our regional citrate anticoagulation protocol is found on the last page of the attached document. I hope this helps.
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Protocols or guidelines for whom it can be used, any exclusion criteria, guidelines for the use of hypothermia blanket and how/when to rewarm.
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I think the key issue here is that we are talking really about two different patient populations. The accidentally hypothermic patient during or after surgery would likely have greater metabolic demands with the increased stress from inadvertent hypothermia and the consequent increased metabolic activity that is generated in order to combat it (particularly with shivering). On the other hand, post cardiac arrest, when there is purposeful induction of reduced temperature (whether you choose 36°C or 33°C, or somewhere in between, based on the current equipoise that exists around goal temperature), with proper sedation and monitoring, oxygen consumption and general metabolic activity decreases.
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I am currently editing a book about critical care nursing.
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Hi Birte,
there is few articles about this topic in ICU, but in the field of research of oncology you can find more aticle on the chidren as relatives. I'm very interested by this topic, i'm working on a similar project, and the goal is the understanding of the psychological impact of the chidren visit. We are working on the literature review. And you, why do you interested by this topic?
Best regards
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Do you think that this technique is superior to CVVHF?
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I agree with Yalim Dikmen and Philippe Mateu that renal replacement therapy in intensive care should be individualized. In cases of hypercatabolic renal failure e.g. it may be necessary to additionly perform conventionel hemodialyses 
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I have Sp02% and Fi02%, and I want to calculate a Pa02/Fi02 quotient. Is it possible to calculate a Pa02 from Sp02%? If yes, does anyone have any reliable formulas?
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I don't think anyone has done any better that Severinhaus' equations.
John W. Severinghaus. Simple, accurate equations for human blood O2 dissociation computations. J. Appl. Physiol: Respirat. Environ. Exercise Physiol. 46(3):599-602, 1979. revisions, 1999, 2002, 2007
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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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GDT has been shown to improve perioperative morbidity asociated to perioperative medicine, but could plethysmographic curve variation (POP variation) become a rutinary valid parameter in this case?
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Perhaps you might like to look at these...?
Lee QY, Redmond SJ, Chan GSH, Middleton PM, Steel E, Malouf P, Critoph C, Flynn G, O'Lone E, Lovell NH. Estimation of cardiac output and systemic vascular resistance using a multivariate regression model with features selected from the finger photoplethysmogram and routine cardiovascular measurements. Biomed Eng Online 2013; 12: 19. doi: 10.1186/1475-925X-12-19. (Designated Highly Accessed via BioMed Central)
Chan GSH, Fazalbhoy A, Birznieks I, Macefield VG, Middleton PM, Lovell NH. Spontaneous fluctuations in the peripheral photoplethysmographic waveform: roles of arterial pressure and muscle sympathetic nerve activity. American Journal of Physiology - Heart & Circulatory Physiology 2012. 302(3):H826-36
Middleton PM, Davies SR. Noninvasive hemodynamic monitoring in the emergency department. Curr Opin Crit Care 2011 Aug; 17(4):342-50
Middleton PM, Chan GS, Marr S, Celler BG, Lovell NH. Identification of high-risk acute coronary syndromes by spectral analysis of ear photoplethysmographic waveform variability. Physiol Meas 2011 Jun 27; 32(8):1181-1192.
Middleton PM, Tang CH, Chan GS, Bishop S, Savkin AV, Lovell NH. Peripheral photoplethysmography variability analysis of sepsis patients. Med Biol Eng Comput 2011 Mar; 49(3):337-47
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What is the real risk of central vein stenosis after short term renal replacement therapy in a critical care unit?
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Just say hello and attach an article source for you to browse
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I am considering to start an animal study on TCD and zero flow pressure but I have no experience on TCD in species other than humans.
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Thank you for your interest in this issue. I've participated in several workshops on neuromonitoring in swine and we use to introduce intracranial monitoring devices during these workshops. From that experience I find that the skull in swine is quite thick and there is no a large temporal "flake" to use as US window. Do you know a US window for the swine?
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Currently working on publishing my study in to the outcomes of critically-ill elderly patients admitted to intensive care.
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Hi Sandra
Thanks for that. I was wondering if there are any tables that actually show the predicted mortality for critically-ill patients based on age at admission.
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Our team suspects that IV amiodarone acute hepatotoxicity does not really exist. We think that the "hepatotoxicity" we can find after the administration of IV amiodarone is more a hypoxic hepatitis related to hemodynamic instability or arterial hypoxemia. Amiodarone just favours the hypoxic hepatitis in case of hypotension during its administration. Something possible due to the solubilizer polysorbate 80. We would like to know your point of view specially related to the cardiac surgery postoperative patient.
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Mohammad Zahidullah sir, thats a very scientific explanation of this problem. a head to head study can atleast give a starter about it.
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It is not infrequent to see chest tubes lying in odd, albeit dangerous positions in critically ill patients when they are imaged (CT scans). What are the factors responsible for malpositioning of chest tubes and what effect this has on the patient course? What is the incidence of such occurrences?
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Dear Manoj, you are right but we have seen fairly large number of chest tubes in dangerous locations viz. paracardiac.
What should we do to decrease this occurrence
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We have a clinical problem with a patient with GBS treated promptly with IVIGS. The EMG examination talks about acute motor sensory axonal polineuropathy (AMSAN) with deteriorating clinical course from the first EMG examination. Now the patient is on mechanical ventilation and has no acute infections. At the moment, they have disautonomy and tetraparesia. 21 days ago they received 2 gr/kg in five days of IVIGS. What would you do now?
Nothing,
A second course of IVIGS,
Plasmapheresis?
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Thanks for all your opinions, but the Guidelines on the Use of Therapeutic Apheresis in Clinical Practice (Journal of Clinical Apheresis 28: 145-284 (2013) says with GRADE methodology that is 2C ( very weak)...
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The nature to which the problem to be looked at within the given area of ICU is what constraints if any contribute to an untimely admission. As this is an area which locally has not been identified as having collected data on the timely admission to ICU, it was an area which needed to be investigated.
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Hi Julie - yes, I see the same in the ED setting, there is a considerable body of literature in relation to aspects of ED and hospital overcrowding, and I think for most specialty areas, where the back flow from high levels of hospital occupancy has resulted in failure of patient flow. It becomes a hospital wide problem (and essential a social problem as well) as wards cannot accommodate the patients from ICU due to their lack of space, which is linked to inability to discharge patients often associated with inadequate or insufficient community support systems. One of the challenges is to address the 'silo' effect that often occurs in health care, where individual areas focus on their own concerns without looking at the 'bigger picture'. It can be difficult to get buy in to processes aiming to improve patient flow, with out recognition that it needs to be a hospital wide approach.
Unfortunately, responses often do not occur until sentinel events raise the profile of the issue, and as you identify this is often in the form of increased mortality. Certainly in relation to ED practice, one of the factors that has led to greater priority in relation to overcrowding has been the development of research that has clearly linked patient outcomes (increased length of stay and mortality in particular) to this phenomenon. It has been shown that failure to be able to move patients on to the more appropriate areas is linked with measurable negative outcomes. I think that the need for such research is one way to highlight the issue and its severity. There also need to be moves ant a socio-political level, with increased public awareness of the issues and the potential outcomes, and a willingness to re-look at the traditional processes and priorities within the health care system. As you so rightly note, with the increasingly aged population, chronic disease and co-morbidities associated this issue will only expand.
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A 82 years old patient undergone to cephalum pancreatectomy developed a biliary fistula with high flow (> 1000 ml/day through drainages) in third postoperative day. After 24 hours hypernatremia (162 mEq/L) appeared. Cardiovascular hepatic and renal function was preserved. There were not signs or symptoms of infection.
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Curiously in this case of acute hypernatremia (162 mmol/l) secondary to a biliary fistula, the RENAL FUNCTION WAS NORMAL..
In clinical practice, it seems very hard to believe.
Two hypotheses.
First. Creatinine values were in the normal ranges but elevated if we consider the age and the body weight of the patient. MDRD creatinine clearance should be largely decreased, and glomerular filtration rate largely overestimated (my favorite hypothesis). In this case, the patient suffered from hypovolemia and severe SALT and Water deficit.
Thus 0.9% NaCl infusion should be the gold standard. It will avoid cerebral thrombosis, correct hypovolemia, total dehydration, and hypernatremia according to the osmolality differences.
Whereas, “renal function was normal”, body water loss calculated by G G Rugierri was of 6.3 L!! It would have been of interest to have glycaemia, serum bicarbonate values and the calculated effectiveness osmolarity (without BUN weight). Furthermore, question’ author should now provides creatinine values before, during and after this acute hypernatremia to confirm this hypothesis.
In case of severe extra and intra cellular dehydration systematically associated with hypovolemia and acute kidney dysfunction, 5% dextrose infusion should be avoided even in absence of gatroparesis, since the patient needs Nacl and H2O.
Formula to calculate water loss could be of interest for academic discussion, but their usefulness in clinical daily practice is still debated. I never used them.
The second hypothesis, eliminated by the author when calculating the water loss, may be of interest. In this case, in absence of acute kidney dysfunction assessed by previous values, hypovolemia and extra cellular dehydration are excluded, thus severe acute hypernatremia should be linked to inadequate post-operative infusion such as important sodium bicarbonate infusion. 5% dextrose infusion should be the best in view of gastroparesis.
Hypernatremia therapy should be evaluated with the extracellular compartment status and therefore the presence or not of acute kidney abnormalities assessed by urine output and RIFLE or AKIN criteria.
To conclude: in case of
- Total dehydration and AKI: 0.9 Nacl infusion, even in presence of confusion.
- Euvolemia and normal extra cellular hydration, linked to therapeutic mistake (!): 5% dextrose infusion in absence of possibility to use gastrointestinal tube, but remember that the risk of central pontine myelolysis is very high, if hypernatremia is corrected too quickly.
PS: 4.5% of saline is not useful and frequently not available, but when infusing 500 ml of 5% dextrose and 500 ml of 0.9% of saline, you perfuse 1000 ml of 4.5 % of saline associated 25 g of glucose: a cook book
HES being a pathophysiologic nonsense should be avoided.
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A 40-year old Filipino man, known to have hypertension for 4 years was admitted to our hospital with severe headache and left sided dense hemiplegia, CT finding was consistent with hemorrhagic stroke. On the tenth day of admission he developed shortness of breath of sudden onset with a significant drop in oxygen saturation. CT angiogram showed saddle pulmonary embolism.
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It's quite dilemma. Regardless the risk stratification, anticoagulation is still indicated.
I would choose LMWH twice daily even in sub-therapeutic dose. A multidisciplinary approach (neurologist, neurosurgeon, cardiologist, haematologist ) regarding the selected anticoagulant and its dose regimen is preferable in this case.
Hope that my opinion would be helpful.
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Is the term ALI is really obsolete after emergence of the new Berlin definition of ARDS ? Whats is the actual purpose of such a definition?
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I've recently read a great Editorial in British Journal of Anaesthesia. See Frohlich S et al (2013), BJA 111(5), 696-9. ARDS: progress unlikely with non-biological definition.
It certainly got me thinking!
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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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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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