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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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Cristobal,
it depends on what you are most interested in. There are scores and ways for assessing workload in bedside nursing that accounts for physical and cognitive workload. Look at work by Heather Tubbs-Cooley. Also, make sure you are looking at the right measures. As I’m sure you know, tools to assess staffing models are not the same as nursing workload. I have partnered with nurse scientists at Emory to look at a combination of metrics, but it also depends on the question you are asking. Hope this helps. Feel free to DM me if you want to discuss further
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At the beginning of each shift, how nurses distribute current patients in the unit?
According to my experience, there several factors that are considered such as if the patient is on ECMO, mechanically ventilated, on a particular isolation precaution...
Also, there are nursing to patient ratios as guidelines but their account for the number rather than specific features of the patient.
Any other criteria or methods?
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Distribution of staff in the ICU depends on the availability of workforce or number of staff in the ward and patient status or it's progress. However, 1:2 is good ratio when there is good help and support for the nurse but if not, so 1:1 is relevant.
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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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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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Platelet transfusion? Desmopressin? rFVIIa? TXA?
Always more frequently in our hospital we have to treat traumatic brain injury in patients receiving antiplatelet medication.
I know there are no unanimously recommended guidelines.
A recent update of european research group on bleeding care in trauma (Spahn et al. Critical Care 2013; 17: R76 -http://ccforum.com/content/17/2/R76 ) recommended:
- to administer platelets in patient with substantial bleeding or intracranial hemorrhage who have been treated with antiplatelet agents (GRADE 2C).
- to administer desmopressin (0,3 mcg/kg) in patients treated with platelet-inhibiting drugs (GRADE 2C).
- to treat with platelet concentrations patient with continued microvascolar bleeding, if platelet dysfunction is documented (GRADE 2C).
Waiting for PATCH study (de Gans et al. BMC Neurology 2010, 10:19 -
http://www.biomedcentral.com/1471-2377/10/19 ), what is your experience about this clinical context? Have you ever used rFVIIa?
Do you measure platelet function in patients treated or suspected of being treated with antiplatelet agents?
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Desmopressin has no significant hemostatic effect in connection with
trauma and massive bleeding but can be useful if there is a simultaneous
platelet function defect or in certain forms of VWD. Desmopressin is often
combined with tranexamic acid.
For dosage and special considerations for treatment
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The neurologic examination is a powerful tool for urgent bedside assessment of ICU patients with neurologic or neurosurgical illnesses. Assessing cranial nerve function is one of the most vital components In this context. Testing the pupillary light reflex evaluates the status of the second and third cranial nerves. Automated pupillometers have been developed that provide objective measures of size of the pupil and the responsiveness of the pupil to light (neuropupillary index). Although few studies reveal diagnostic and prognostic usefulness in critically ill patients, none of the studies correct/adjust for interfer and confounding effects by for example sympathomimetic or parasympathomimetic drug effects, interference from ambient light, previous cataract operation, etc.
Isn‘t it much too early to reliably use automated pupillometry for diagnosis and prognosis in daily clinical practice in ICUs?
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The size of the pupil, and the responsiveness to light is definitely a key procedure in neurological ICU patients (especially concerning intracranial pressure) as many of the other neurological tests require active participation of the patient. However automated pupillometry has not found the way to our ICU and I think that the amount and quality of studies is not sufficient yet. In my opinion, it's a great approach, as manual pupillary examination shows a great variety between the investigators. On the other hand, many critical ill neurological patients have a external ventricular drainage anyway. So I think more and larger studies are needed, if they show positive results, automated pupillometry could assist the examination in future.
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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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What is the effect of cardiac arrest on GI perfusion?
What are the short term (acute) consequences of cardiac arrest on GI function?
If someone were to restore spontaneous circulation, would the gut have taken a significant enough beating to not be able to well absorb an oral medication for example?
Thank you
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Mouse models of endotoxemia (such as an LPS injection) are associated with increased cell death. Such as increases in cell death seen in the spleen.
In human patients with endotoxemia I think cell death is also observed. However, I am unsure where it occurs, to what degree, what cells? What similarities are there to the mouse model?
I would assume there is. However, I don't know any critical-care clinical pathologists to whom I can pose this puzzler.
I can mention that this 12 year old article by L. Moldawer makes reference to cell death in humans; http://www.fasebj.org/content/15/6/879.long Back then it was of course referred to as apoptosis. Which, IMO is a just a general term used by many people for cell death.
What new information is out there regarding cell death observed in humans? Are there any existing treatments which attempt to address/prevent cell death in human clinical endotoxemia (assuming it is looked for)?
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Agree with Hans-Dieter Volk. In contrast to murine endotoxaemia, in human no standardization may be achieved. We had several studies of LPS, EndoCAb, cytokines, and apoptosis markers as well, etc. in both humans and rats. Comparing is difficult as humans have disease status when raised LPS is only a part of condition, while in rodents we use industry made LPS with standardized source, activity, etc. PCT, lactate, total cholesterol or other markers are useless when trying to achieve direct effect of LPS. Furthermore, LPS-binding protein influences the pro-apoptotic effect of LPS multiple times. Same levels of serum LPS under different conditions (for example, sepsis, IBD or fatty liver disease in our studies) cause different levels of apoptosis.
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Please take part to this international survey (3 minutes!). We want to know how you manage anticoagulation, including antithrombin supplementation, during veno-venous ECMO. Your contribution will be acknowledged in case of publication (this is why the survey is not anonymous).
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Dear Alessandro Protti,
VV-ECMO- Veno-Venous ExtraCorporeal Membrane Oxygenation is an artificial Membrane Lung, with its blood pump, placed in series with the failing Natural Lung (NL). The ML can totally or partially take over the functions of the NL in both carbon dioxide removal and oxygen intake. The delivery of O2 to the patient's metabolism and the removal of CO2 depend on a complex interaction between the ML, the NL and the metabolic status. Why anti-thrombin (AT) is needed during VV-ECMO?
-Bleeding is the most feared complication during ECMO and is associated with high dosing of heparin. Although, there is no consensus on antithrombin (AT) supplementation during ECMO, AT is needed by heparin to properly anticoagulate. Heparin is required during ECMO to avoid circuit thrombosis and its anticoagulant effect is strictly dependent on antithrombin (AT). AT also plays a central role in mediating inflammation. Acquired AT deficiency is common in patients on ECMO, arguably due to long term anticoagulation in addition to sepsis itself. AT supplementation increases anti-Factor Xa (anti-Xa) levels without increasing heparin dosage. This may have a clinical impact because risk of bleeding during ECMO is associated with higher heparin dosage. Clinicians strongly believe that maintaining normal antithrombin activity levels (80%-120%) during ECMO will potentially be associated with:
1. Less heparin dosage
2. More adequate level of anticoagulation
3. Less hemostasis related complications, and
4. A lower level of inflammation
See the links below:
Best wishes
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Whether we use in operating rooms or in intensive care for various reasons and with acceptable cuff pressures
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It depends on the scenario behind the case. Among emergency cases, If the patient is a difficult case of intubation , it should be remained until an alternative definite airway management is ready to perform.Among the elective cases, it should be applied only for minor surgeries with an expected duration time of less than 30-45 minutes.
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How frequently have you observed this phenomena ?
Is this rather rare or maybe quite common ?
Has there been any research done investigating this specific circumstance ?
We are currently investigating the correlation between ultrasound of the inferior vena cava during haemodialysis at three time points (start/middle/cessation) in comparison with simultaneous blood pressure readings and predialytic bioimpedance measurements.
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As Dr Smith has said above,this is a very common issue.
Patients on maintenance haemodialysis,especially those who are oligo-anuric,oscillate between being effectively underfilled post dialysis,and over filled when approaching dialysis,and are very often concurrently hypertensive.
The hypotension following induction of general anaesthesia in that group of patients can be both marked and rapid.
Clearly,volume expansion is not an easy option in anuric haemodialysis patients,and use of vasoconstrictors such as metaraminol or phenylephrine is often required.
Best regards,
Ian
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I am looking for recent (2012 to present) case studies, research articles, etc on the use of double sequential defibrillation in terminating refractory ventricular fibrillation
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Blood Lactate  and Lac time is a good diagnostic and prognostic tool in ICCU and ITU.. Can anybody share its role in neonatal Sepsis?
one article: Journal of Emergencies Trauma and Shock 10(2):55 · January 2017
DOI: 10.4103/JETS.JETS_103_16
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Yes I have gone through it today. This is very useful paper. Thank you so much Dr Mansour.
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Is there a positive effect on parallel canullamanegement and the weaning of ventilation? Or is there to less evidence of effectiveness?
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Less sedation, better suctioning, most probably earlier separation from the ventilator.
Tracman study compared early versus late trachy, where no mortality benefit had been shown
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Ivabradine, beta blockers, negative inotropic effect, HOCM, research paper 
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Thanks James for your answar. Beta blocker, verapamil and disopyramide are generally used to treat HOCM. Few studies are available to evaluate the role of ivabradine in HOCM in cat as you mentioned .I think human study is needed with this molecule where beta blocker are contraindicated like associated severe COPD. 
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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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According to NCBI guideline, it is recommended to administer maintenance IV fluids required by the patient (30-40ml/kg/day) during day time to ensure good sleep for the patient and nurse. But this guideline didn't mention maximum accepted infusion rate for maintenance IV fluid !!! so how much maximum accepted rate  and what are the possible complication if it is exceeded? 
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We can't fix a maximum rate for i.v. infusion. either for adult or children, it is a multifactorial and has to be adjusted according to the patient
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Is there any guideline or published papers regarding the use of maintenance IV fluids in patients with fluid overload (eg. CKD or HF) who are already using diuretics to relive symptoms of pulmonary congestion?? 
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If they have any pulmonary issues secondary to hypervolemia, fluids are not indicated. However, if you are talking about a stable CHF patient with chronic diuretic use who needs maintenance therapy for whatever reason, 5% dextrose in a solution of 0.9% saline is acceptable at modest rates amounting to the fluid restriction they have been following as outpatient (~1.5L per day).
You may want to go through this article.
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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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I need to refer to a range of normal PaO2 levels during CPB in a new manuscript I am preparing. Are there any guidelines or textbook chapters referring to a "target values of PaO2 during CPB", e.g. 150-250 mmHg?
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Your right on. Looking forward to reading your paper.
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In a very disturbing outcome last week, a young woman was found unconscious in her car on Staten Island in New York City. The responding police took her to the nearest ED (SIU Hospital) where the treating physician correctly diagnosed opioid overdose, and administered naloxone. The pt became conscious, and was discharged into police custody 6 hours after receiving IM naloxone and showing "healthy" vitals. She was incarcerated and died a few hours later in jail of an opioid overdose. My initial reaction was that 6 hours is not enough time to be certain that an opioid OD pt is stable and ready for discharge, but after reviewing the scant literature on the subject, I found articles like the one attached (NEJM) stating just that - administer naloxone, wait six hours, if oxygen sats and HR and BP are fine, then discharge. Of course, this presumes many things, predominantly that the pt has ODed on a short-half life opioid like diacetylmorphine (Heroin) and not a long-half-like one like methadone (which could explain the tragic consequences of last week). Conceivably, a pt could OD on a long-half-life opioid, be revived by naloxone, and then die of respiratory depression as bioavailability returned. Does anyone know of any newer (DOI: 10.1056/NEJMra1202561) and more nuanced protocols for the treatment of opioid ODs in the ED?
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Although I was not able to find any newer protocols for the treatment of overdoses in the emergency room, I have a few comments I would like to make about tragedies such as this and the linked guidelines.
First, while the flowchart in the NEJM article mentioned the consideration of discharge after 4-6 hours of observation (post naloxone infusion given the obtainment of normal vitals), the supplementary writing suggests that 12-24 hours of care are needed when a continuous naloxone infusion is administered. It is interesting, that both yourself, and the health professionals treating the deceased patient, both cited/exercised 6 hours of observation. While you noted the apparent inadequacy of this; the treating physicians deemed this acceptable. The treating physicians were most likely familiar with these guidelines which seems to suggest a very real danger of a paint-by-numbers approach to medicine. Instead of recognizing the caveat printed in the NEJM article, most individuals appear to simply focus on the algorithm presented.
Second, a few things about the events leading to the death of the patient. It is odd, that during the 6-hours of observation, the guidelines do not place a specific recommendation for the use of toxicology screening to identify the specific opioid or the presence of polysubstance use. Maybe the physicians who treated the deceased patient performed this screening, but this seems unlikely as people love to report on the atrocities caused by specific opioid agents. Also, I would like to know why this person was arrested and incarcerated. Unless she had some quantity of illicit drugs on her person, there doesn't seem to be cause for arrest. It is disgusting that law enforcement officers view drug users as criminals and circumvent reasonable thought in order to get a pat on the back from extreme teetotalers (unless of course there was a legitimate reason for arrest). Additionally, why was this woman allowed to die in the jail, did nobody check on a compromised inmate who was just released from the emergency room for a drug overdose as few hours ago? While respiratory depression (maybe?) was the means by which the patient/inmate died, the real cause of death appears to be negligence. 
Third, the most reprehensible thing in the passing of the unconscious female motorist, was her opioid overdose was extremely treatable (as evidenced by this person’s temporary recovery). This is the real tragedy of these deaths; they can be easily prevented. At this point, I need to rant on the ramifications of sensationalizing deaths resulting from opioids. Thanks to the superfluous war on drugs, people seem to views occurrences such as this as proof that these substances are a treacherous societal scourge. This is a major component in the push for physicians to avoid the use of opioids/opiates in treating patients. This is foolishness and other analgesics (NSAIDs, acetaminophen, etc.) are similarly dangerous (though possibly less fatal [Solomon et al., 2010]) and, therefore, do not make the choice of pain management any simpler.
Most of this content is somewhat irrelevant, but I just thought I would share my views on the failings of overdose management. I am glad to see that someone (you) recognized the insufficient guidelines in treating these occurrences.  
References: 
Solomon DH, Rassen JA, Glynn RJ, Lee J, Levin R, Schneeweiss S. The comparative sagety of analgesics in older adults with arthritis. Arch Intern Med. 2010;170(22):1968-1978.
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My project is to evaluate the LVEDP in trained vs untrained/deconditioned individuals. I don't want to cath the subjects. Is there an accurate way to measure the LV filling pressures? Thank you.
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Thomas is absolutely right, but your study poposal is different, because you want to see if there is any influence of training on LVEDP, and not to sepparate between normal and disturbed diastolic filling patterns. You are trying to sepparate lets say in otherwise healthy individuals between an LVEDP between 5 and 12 mmHg. In general TDI and conventional doppler may separate below and above 15 mmHg. Most important to me seems to have an absolutely sound study protocol. 1.) TDI and doppler parameters are age dependant (so you have to choose a quite narrow age margin (not more than 10 years, e.g. 15 to 25 years of age) 2.) perform all exams on the same machine and with the same technician (or by yourself) and the same condition (time of rest before exam), left shoulder recumbency etc....) 3.) if you suggest a LVEDP difference between the groups of 3 to 5 mmHg and you have an error of 3 mmHg (interobserver variability and day to day variance, and intraobserver variability and interindividual variability) you will need at least 50 probands per arm to detect a difference of 50% of LVEDP (e.g. 5 mmHG versus 7.5 mmHg), is the difference between training conditions less, you will need even more probands.
Best
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my patient is 24 years old person , he has tracheal stenosis and stem bronchus  stenosis , could it be tracheal hamartomas  ?
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he has been hospitalized in intensive care unit for few days because of loss of consciousness due to an  obstruction , he reported also a chronic dyspnea in last few years
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Bronchoscopy is a very important adjunct in the practice of ICU, however it was not part of my ICU training. Can you suggest some good places for a visiting fellowship or hands on course on paediatric bronchoscopy?
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I haven't worked in London for several years, however if your keen to experience progressive and pro-active work its a City worth visiting and working in.  I used to work in adult ICU, however a number of colleagues specialised in paeds. If your looking to move then its worth looking up London Hospitals, and recruitment is always ongoing
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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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Ultrasound has been used for different functions, what is its role in the diagnosis, evaluation and evolution of intra-abdominal hypertension?
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I have not seen such report yet. however, several parameters may be helpful such as distension of inferior vena cava, need exclusion of volume depletion.  
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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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Some critical ill patients were very sensitive to vasopressor drug like dopamine or norepinephrine even though these patients has a euvolemia?
How can we explained these phenomena?
These patients usually has a normal cardiac function and adreanl function.
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Hi,
the individual patients' response to vasopressors can indeed be very variable. Firstly, patients will have a varied individual response of their end-organs to catecholamines. Secondly, you will also have to take into account the patients' endogenous sympathetic response. For example a young, otherwise healthy patient in let's say, septic shock will have already mounted a significant adrenergic response with a relative less pronounced response to exogenous catecholamines, whilst an elderly patient may have not been able to mount this response themselves and will respond far more to the administration of pressors. 
Best wishes,
Immo
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24 year old man with deforming arthropathy and limitation of hip movement. He also has features of aortic stenosis and allergy to food in a way that he develop vomiting from certain foods with irritability, impairment in memory, forgetting, and nervousness.
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Careful assessment of AS severity. Consultation at a center with experience in percutaneous approaches to management of aortic stenosis.
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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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Hi All,
I have seen many House Officers, Medical Officers, Registrars and even Consultants finding difficulties in inserting IV plug on small vein patients.
It is normal to have EN or SN to do them but these days, such skills are rare.
What happen during emergency if none have the skill to just insert a mere IV plug when the only medicine route is by IV?
And some of them are "famous" surgeons too .. imagine how accurate they could be when a mere small vein they could not find ... scary indeed.
Best regards - Mariam
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Dear Hulya,
True enough, such are the practices but most often - even the protocols does not work at all.
I respect those junior staffs more than the HOs, MOs, Regs, Consultants and some even Surgeons (not all) who could not even find a single IV line in just one shot some in ED environment especially.
I once saw the cardiac catherization surgeon prod blindly the catheter despite using guided fluoroscopy and went into force blocked elbow and shoulder owing to sadistic personality disorder.
Another was few MOs finding lines going over all four limbs on a poor patient for 5 times each (that's 20 useless shots) simultaneously for a mere MIBI procedure leaving the patient faint during the painful episode.
The sad thing about the one I saw right under my nose was the fact that few MOs and Reg trying to insert a mere IV line for a Code Blue GCS 3 patient to no avail. On the 30th time after a 5 hours attempt using Ultrasound machine only then the saline gets working together with other blood tests and medications. Imagine if the patient has heart attack and needed the necessary IV medication, he would have long died without any help from these so-called "professional experts".
Those with basic practice is never sharpened nor there at all but hiding behind the vast brainy knowledge and bragging alone (not all) with no skill to boast of except to lecture their juniors into performing what they lack for fat paychecks. My main worry is what if they are surgeons and they cannot even find the right vein or differentiate the artery in open surgery and cut off everything in the name of science and experiment. Sounds ridiculous but it happens in our daily lives.
It is truly a Hitler-like era where everything is experiment under the guise of perfection. Sadly, this basic skill is still not a requirement to pass any basic, intermediate or advance module for mere medical study in my (?) country, pathetically. It is the immediate diagnosis which is most important and never the need to medicate urgently.
If a simple IV line cannot be simply inserted, what about central line, jugular line and all the important lines save those easy intraosseous jab that any non-skilled paramedic can initiate just like uneducated insulin-jab patients could do.
That much my concerns and sympathy lie.
Best regards - Mariam
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If i encounter a case of gunshot with a foreign body in the chest  and the patient is stale after chest tube drainage shall i remove the bullet?
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This problem was studied extensively during and after WWII.  Still, if there is no specific complication, e.g., hemoptysis, bronchial obstruction, infection, it may be left alone and simply observed over the years.  Certainly, I would not operate shortly after the chest tubes were removed, assuming none of the above complications.
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APACHE IV scoring has been implemented for about 8 months.  A recurrent issue is when patients without much chronic health history, but very poor neurological recovery after cardiac arrest are scoring to be very likely to recover.  Is this a known issue or do we need to tweak our calculations in EHR?
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Consider that APACHE is about survival which does not imply neurological recovery.
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WE HAD A NEW CT WITH ORAL CONTRAST. ATTACHED BELOW THE IMAGES. She is ALmost totally obstructed clinically. OGD done but failed to pass this obstruction. What is your diagnosis and advice of management knowing that she is now > 6 months post trauma, well built, good chest, refusing surgery
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DEAR PROF. TENG AND SCHMEDEL
BOTH LUNGS ARE FULLY EXPANDED.   RE OGD AFTER THIS COntRAST STUDY  was able to dilate the esophagus to 10 . there was no diverticulum which was suggested by one of our radiologists
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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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We've recently had a case. Systemic oxygen consumption and extraction progressive decreased while refractory lactic acidosis progressive developed (likely due to mitochondrial "poisoning"). Anyone willing to share data on other cases to write something interesting together? 
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Linezolid-Induced Lactic Acidosis
N Engl J Med 2003; 348:86-87January 2, 2003
Linezolid is an oxazolidinone antibiotic used to treat a variety of gram-positive infections, including those due to methicillin-resistant Staphylococcus aureus and vancomycin-resistant enterococci, as well as nocardia species.1,2 Lactic acidosis is an adverse effect that has been associated with other drugs, including metformin and the nucleoside reverse-transcriptase inhibitors,3 but not with linezolid. We report a case in which severe lactic acidosis developed as an adverse effect of linezolid treatment.
A 52-year-old woman presented with fever, chills, and a two-week history of intermittent cough. Computed tomography (CT) of her chest revealed an infiltrate in the right middle lobe, as well as mediastinal adenopathy. Nocardia otitidis-caviarum was isolated from bronchoalveolar-lavage fluid as well as from a mediastinal biopsy specimen. Additional CT scanning revealed disseminated disease with involvement of the brain, kidneys, and adrenals.
The patient was initially treated with trimethoprim–sulfamethoxazole but had serious side effects that necessitated discontinuation. She was subsequently switched to linezolid and clarithromycin. Her treatment was complicated by myelosuppression, nausea, and vomiting, and gatifloxacin was substituted for the clarithromycin in the hope of relieving the nausea. During the subsequent five weeks, she had persistent vomiting and ongoing myelosuppression. Endoscopy revealed duodenal ulcers, and pantoprazole was started. The patient was hospitalized for intractable nausea and vomiting after 11 weeks of treatment with linezolid and 5 weeks of treatment with gatifloxacin. The findings on repeated endoscopy were normal. The patient was euvolemic and received intravenous fluids during hospitalization.
Because she had low bicarbonate levels, the patient's lactate level was checked and found to be more than 9.9 mmol per liter. Both antibiotics were stopped, resulting in a normalization of lactate levels at 1.4 mmol per liter after 10 days. Both antibiotics were then restarted, but the lactate level measured seven days later was 4.8 mmol per liter. Her nausea returned. The gatifloxacin was discontinued, and the lactate level had increased to 6.5 mmol per liter one week later. Discontinuation of linezolid resulted in normalization of the lactate level after two weeks. There were no other changes in medications during that time. The patient was then treated with moxifloxacin. Her lactate levels remained normal, and the disseminated nocardiosis resolved.
Lactic acidosis is a toxic effect of linezolid whose mechanism is unknown. Other drugs, including metformin and nucleoside reverse-transcriptase inhibitors, have been associated with lactic acidosis. In the case of nucleoside reverse-transcriptase inhibitors, lactic acidosis is thought to involve mitochondrial toxicity,4,5 and linezolid may have a similar effect. As we report here, a potentially serious side effect occurred in a patient receiving linezolid. The serum lactate level in patients taking linezolid should be measured if they have nausea or a low serum bicarbonate level.
Regards
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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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Trying to gather resources for standardized or widely accepted assessments used in the rehabilitation portion of burn care.
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The protocol of rehabilitation is divided in three stage acute, subacute and chronic,
It is expalening in my research you can see that in journal were it is publich
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The guidelines recommend change each 72-96hs in the overall patient, and every 48 hours in patients with COPD, but the practice is very different between different hospitals
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Attached are clinical practice guidelines promulgated by the American Association for Respiratory Care
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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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Can we adapt the strategies in brain injured patients?
In a recent pilot study, Werndle et al. presented preliminary data of a new technique for the continuous monitoring of spinal cord pressure and the corresponding spinal cord perfusion pressure (Crit Care Med 2014;42:646–655). Their analyses revealed that the use of inotropic drugs for an increase of spinal cord perfusion pressure optimizes neuronal function measured by motoric evoked potentials and muscle strengths below the spinal level of injury.
Are we ready for a routinely monitored management of spinal cord perfusion? 
Which mean arterial blood pressure should be targeted in this context?
How long and how invasive should we monitor?
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Indeed, a fascinating topic. Thank you Dr. Sutter to bring this up. I came across a recent article by the Cambridge/London group that has enormous experience with ICP. Intra-spinal cord pressure seems to be closely matched to epidural pressure at the level of the lesion in spine-injured patients, which would make pressure monitoring less invasive and still reliable. Regarding spinal perfusion pressure, the evidence being gathered is most convincing for a principle analogous to CCP.
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Whereas in the ninety’s blind nasotracheal intubation (NTI) was the gold standard for medical ICU’s patients (more than 90%; Vassal et al, Intensive Care Med 1993) and the surgical ICU’s patients suspected or requiring mechanical ventilation more than 48 H (Aebert et al Intensive care Med 1988), after the implementation of rapid sequence induction (RSI), NTI’s use became confidential (less than 1% in a recent survey). Therefore, NTI is no longer taught in the ICU’s, whereas it may be necessary in some particular cases (inability to open mouth, to move the neck…) and reduces at least the risk of unplanned extubation. Moreover RSI is not so safe and easy according to the recent meta-analysis of Hubble et al (Prehosp Emerg Care 2010).
So should we save nasotracheal intubation?
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  • Its a very good question. Now a days, in today's Anaesthesiologists blind nasal intubation (BTI) is a dying art. Its a great technique in the armamentarium of anesthesiologist specially in the scinario of NIL mouth opening and there is a lack  of advanced airway gadgets ( FOB ) at your centre. In some of Asean countries, even now FOB is not available in 60-70 % teaching Hospital. In the given scinario, it becomes  a greatly useful technique.
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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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Failure to rescue is shorthand for failure to rescue (i.e., prevent a clinically important deterioration, such as death or permanent disability) from a complication of an underlying illness (e.g., cardiac arrest in a patient with acute myocardial infarction) or a complication of medical care. Failure to rescue rates used for both research purposes and as quality indicators are typically derived from hospital administrative databases. However, it is not clear how identify it, so what are the best indicators to measure it?
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I also think that retrospective analysis is the only option. Is it accurate to limit failure to rescue to cardiac arrest? Perhaps one of the early warning system frameworks (EWS; http://www.ihi.org/resources/Pages/ImprovementStories/EarlyWarningSystemsScorecardsThatSaveLives.aspx) could be used to expand the conceptualization of "failure to rescue" . It seems that failure to respond, or a delay in response, at any point when the evidence (i.e., vital signs, O2 sat) suggests an intervention could be on a continuum of failure to rescue.  
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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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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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I am doing a prognostic meta-analysis to investigate whether anion gap (a biochemical marker) can predict short-term mortality in critically ill patients. While the effect measure I am mainly interested in is odds ratio, many studies have instead reported the area under the ROC curve (AUC) as an effect measure. I am aware that AUC is a mainly a diagnostic statistic but I was wondering whether it would be appropriate to pool AUCs for this purpose?
Thanks!
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Hi Stella,
As often: it depends:
Although AUCs adequately reflect the overall discriminitative ability of a test or marker, it has little value to inform about the clinical value of a test - who is likely to die and should be subjected to some intervention and who is not. However, the same holds for the odds-ratio.If your aim is to obtain this general discriminative ability of this marker, AUCs could be used as an alternative.
For clinical use, however, it would be more interesting to pool sensitivities and specificities; these are more informative how well the test can identify those who will die and/or those who will survive. But then these prognostic metrics should be reported in the original studies, which may not be the case if they only report AUCs.
Hope this helps.
Regards, Brent
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Termination of resuscitation rules for EMS bls+aed providers (when there is no ALS on scene) are in use in several countries. Does your EMS system use them? Do you have results? How do they work in work EMS Systems? I'm collecting data and trying to validate their use in Portugal. Thank you for your collaboration.
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The on scene senior clinician, usually paramedic, follows local and national (NICE) guidelines to terminate on scene. This is where ALS has proven to be without positive effect and no ROSC achieved but there are also other factors. Children, hypothermic patients etc are conveyed to an appropriate facility for further intervention and are very rarely, if at all, pronounced 'life extinct' on scene.
As to BLS terminating on scene without an ALS provider attending; I feel that is an awkward and maybe a little dangerous situation, to be caught up in.
Personally, I would not cease CPR if only BLS was being attempted.
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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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I'm interested in confirming that metformin intoxication is associated with diminished oxygen extraction and consumption (secondary to mitochondrial "poisoning"?). This can be the primary explanation for concomitant lactic acidosis.
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Dear Alessandro, we treated a female with documented metformin intox several weeks ago. Clinically we observed an increase in pulmonary vascular resistance with concomitant RV failure. The LV was severely hypovolemic. Inhalation of NO did not change the situation. The clinical pictures was comparabale to acute pulmonay emboliism which we ruled out by CT scan. There was also no clinical hint towards RV infarction as systolic RV function was preserved. SvO2 was reduced in this situation. Unfortunatly, as metformin intox is associated with a high mortality our patients also died. Interestingly until her death RV dilation and paradoxical septal motion remained. Therefore one might conclude that metformin persistently interferes with PVR regulatory mechnisms. Greetings from Berlin, ST
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Traumatic brain injury, even in its mildest form, is known to result in degenerative processes including demyelination and dysmyelination of the axons over time. The shearing and tearing of the axons (primary injury) due to the acceleration and deceleration force of high velocity impact would also normally trigger off the secondary injury cascades. This includes the synaptic deregulation, cell death and axonal degeneration.  
But how quickly does these processes start (especially the demyelination of the axons) in patients with mild TBI? I am of the opinion that it will take at least a few days or weeks before such degenerative process starts. What are your thoughts?
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Dear Timothy Shea,
The "miserable minority" are those patients with mild traumatic brain injury who continue to experience prolonged cognitive deficits even after months and years, way beyond the average cutoffs (which is about 3-6 months post trauma).
You were absolutely right that one should consider preexisting comorbidities/(maybe even age) factors and as well as neurobehavioral/ neuropsychiatric condition arising from the trauma that could adversely influence the cognitive performance of these patients. Having said that, there are many studies (Ref 1-5) that has proven that even when all these factors are accounted for, and removed from the analysis, these individuals continue to exhibit deficits in their neurocognitive functions. So what then would best explain these manifesting derangements/ impairments ?
One possible explanation may lie in the structural changes. Patients with visible injuries -complicated mild TBI (radiologically visible lesions  i.e hematoma, contusion, edema, etc) and the corresponding functional and cognitive deficits are findings that are widely accepted by scientific community. How about the wider group of mild TBI patients whose radiological findings are usually negative and discharged from the ED without even being seen by neurosurgeons and without any subsequent follow-ups? Does normal CT/ MRI in the acute stage means there isn't any injury to start with with?
Many advances imaging protocols have proven otherwise. Diffusion Tensor Imaging (DTI) studies (reference to which I will give at the end of this reply) for example are able to pick up changes to the microstructure like the axons or the white matter tracts which are usually missed by the CT/ conventional MRI sequences. Could these structural anomalies/injuries then  explain the neurocognitive impairments experienced by the "miserable minority"? I guess the answer would be affirmative (see ref 5-8). With all these new evidences of microstructural abnormalities (even at the earliest hours post trauma), we can no longer reject the patient experiences as purely psychogenic in origin, ensuring we do our due diligence. 
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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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We distributed the recent AAP guidelines for the management of bronchiolitis to our pediatric group but still find the inertia of routinely administering albuterol hard to reverse. What is the international experience?
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Here we experience the same problem. As we have no proper therapeutic measures to apply, we end up administering salbutamol (in our case) to almost all infants. However, we've been using saline in almost all cases, with apparent good results. 
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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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Do you think procalcitonin is a useful tool for early discovering the post-traumatic septic complications? Has anyone ever tried to assess the increase in plasma current day / day before?
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again, as my forespeakers, i would like to highlight theimportance of s e r i a l pct measurements in the trauma patient. The extent of pct secretion of the first 24 - 48 hr is likely to be related to the extent of trauma itself, as well as to other factors influencing this value, like duration or intesity of surgery. Therefore, obtained pct cut-off values of the before mentioned studies lack external validity. One has to keep in mind that in trauma patients not only septic insults, but also other events (like re-surgery, or newly developed circulatory shock of other than inflammatory causes, just to name two of them) can cause pct elevations, or alter the expected decline of pct. Every single pct value has to be carefully evaluated in the clinical context of every single patient.
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Male patient, 46y motorcycle accident. Cardiac arrest at the scene for 5 min. Whole body CT with thoracic trauma only. Flail chest from 2nd to 7th left ribs(CT attached). Eco: normal. 5th day after trauma still in the ventilator. Fever from a probable pulmonar infection. Had an air leak until day 3, now there is no air leak. Would you perform an titanium plate (I'd use the MatrixRib system) fixation procedure in this case? Can we put those plates in patients with systemic infection?
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I would prefer to avoid the prosthetic material in already infected patient.
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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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We use SimMan 3G (tears, blinking, sweting, tonic/clonic (every 20 seconds) and RR 60/min + artificial ventilation).
The patient is intubated "5minutes ago"  RSI in intermediate care for respiratory failure, propofol + sux are over ...
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Seth brings up an important topic: how to teach mechanical ventilation using simulators. There is virtually nothing in the literature that is devoted specifically to this topic in a comprehensive manner.
Some basic information can be found in the fist two volumes of Respiratory Care journal in 2011, which were devoted to articles on patinet-ventilator synchrony - 2011;56(1&2).
See also these articles:
Mireles-Cabodevila E, Hatipoglu U, Chatburn RL. A rational framework for selecting modes of ventilation. Respir Care. 2013 ;58(2):348-66.
Chatburn RL, Khatib ME, Mireles-Cabodevila E. A Taxonomy for Mechanical Ventilation: 10 Fundamental Maxims. Respir Care 2014;59(11):1747–1763.
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We do Teamevaluation and use the ESI Triage Score. Early Warning Scores are recommended for Patients onwards but not in ED. Is it usefull to use them early in the ED, especially before transition. If the cutpoint is reached we could stop the transition to make a reevaluation or maybe an ICU transfer.
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I have felt that the MEWS (Modified Early Warning System) for adult ED patients is a great tool for early detection for patients who may require the activation of the Rapid Response Team.  PEWS (Pediatric Early Warning Scores) is also effective and specific to the pediatric population.  These scores are not yet but should be a standard for any patient who is being admitted or transferred to another facility with continual updates in the score in order for early detection of any deterioration in a patient's physiological status.
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I'm skeptical, especially as I have refereed a lot of low quality research. However, a conversation with a colleague led me to think that there may be some niche (maybe AKI or research in certain parts of the world?) not currently covered by journals. What do you think? Are there particular forms (e.g. online only, with discussion forums etc.) that you think could enhance nephrology journals?
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I feel there is no need for a new Journal, however the need of the hour is to get more data from countries like China. Being not so accomplished in English or other European languages many countries are not reporting interesting data. Instead of adding new Journal we should strive for bringing out more quality data from such countries. It will also be interesting to see if we can change the policies in dialysis particularly as the current data is heavily based on Caucasean population studies.
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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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Do you follow blood conservation/transfusion guidelines in perioperative care in cardiac surgery? If so, do you use known international/regional guidelines or an institutional protocol?
What are important points in the development and/or implementation of an efficient protocol for blood conservation/transfusion?
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Why not?
Make another three possible and simple questions:
one) who can justify the "unversal" transfusion of the "two units pack" of red cell concentrates?
two) who can justify that a patients admitted at the surgical waiting list during months could come anemic to the operation room?
three) who can justify to do not use autologous blood? why do not recover intra or post surgical bleeding and reinfuse after wash it?
Please, do not ask if we follow, ask youself why you do not follow the blood management guidelines?
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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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Dual modes of ventilation seem to be more physiological.
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Although we also consider PRVC our mode of choice for the previously stated reasons, it also comes with some caveats. When using lung protective strategies during ALI or ARDS with tidal volumes adjusted for PBW, it is not uncommon for patients to generate tidal volumes far greater than the set parameter. This may cause a decrease in mean airway pressure, thus affecting oxygenation. I also believe the jury is out on whether spontaneous volumes greater than 8 cc/kg lead to VILI despite the low plateau pressures generated by spontaneous efforts. Does this make APRV a better option?
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For example skills of anesthesia (intubation, use of curare and hypnotic drugs), emergency surgery (chest tube, tracheostomy, caesarean section), orthopedics (external fixation pelvis and long bones), ultrasound.
I think it is important to define the core competencies essential to a physician who works with low resources in a developing country. This will have to be the basis of sustainable training.
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ATLS ;-)
Did anyone mention radiological skills yet, in the suggested setting particularly conventional X-Ray.
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I think it's not feasible, but someone else doesn't agree.
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If they need analgesia, they don't need CPR; if they need CPR, they don't need analgesia.
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Here's a better link for the first method mentioned above, it's also available here on RG. A couple of other methods are also published using either LC-MS or HPLC-UV, so you can just make your pick based on which equipment you prefer or have available. What you need to be sure of is that the method does not allow uncontrolled hydrolysis of CMS into colistin during sample work-up as is the case in microbiological assay methods and at least one HPLC based method.
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With some of our septic patients experiencing acute renal failure needing CVVHDF, I have posed the question, that as yet I can find no answer to.
With 'normal' patients in ARF on CVVHDF, they would become hypothermic to a temperature of 35 Degrees or below. Hence needing active warming through a Bear Hugger and filter heater aids.