Science topics: MedicineAnesthesiology
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Anesthesiology - Science topic

A specialty concerned with the study of anesthetics and anesthesia.
Questions related to Anesthesiology
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Please share your experience.
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Semi-inflated
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Awake craniotomy and related anesthetic techniques in the operating theatre
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This is "my topic"!! There are several anesthetic options (please see attached our editorial in BJA )
Asleep-awake-asleep approach with selective scalp block looks to be the best option: craniotomy is painful and general anesthesia with LMA during that step is highly comfortable for patients.. Propofol and remifentanil, specially with TCI, guided by processed or raw EEG, allows a very close titration of drug doses and fast intraoperative awakening ( PMID DOI: 10.1097/ANA.0b013e31805f66ad).
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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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Is there a current consensus on the causes of postanesthesia (IV) shivering? Based on a quick scan of articles, an early primary assumption (c. 1980-90) was that it was due to low body temperature, but more recent articles suggest it might be due to something else / multiple factors.
From this article: Lopez, M. B. (2018). Postanaesthetic shivering–from pathophysiology to prevention. Romanian journal of anaesthesia and intensive care, 25(1), 73. Full text:
"Shivering is usually triggered by hypothermia. However, it occurs even in normothermic patients during the perioperative period. The aetiology of shivering has been understood insufficiently. Another potential mechanism is pain and acute opioid withdrawal (especially with the use of short-acting narcotics)."
Thanks in advance for any comments.
Catherine Baumgartner
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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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Standard precautions are meant to reduce the risk of transmission of bloodborne and other pathogens from both recognized and unrecognized sources. (WHO) It is also recommended to assume that every person is potentially infected or colonized with an organism that could be transmitted in the health-care setting and apply the following infection control practices during the delivery of health care. (Guideline recommendation). Personal Protective equipment are to be used as one such measure. But I am unable to find whether the OT table and floor should also be covered with plastic? Please give your opinion with logic (reasoning) and evidences.
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The built environment should be appropriate to allow cleaning and disinfection e.g. Impervious and intact surfaces for floors , walls , coverings on the mattresses, that allow ease of cleaning and prevent ingress. The principles of environmental decontamention after any patient is based on cleaning then disinfection if needed Including after spillage of blood or body fluids or patient known to be infected e.g. MRSA! CPE etc . All medical devices which includes the theatre table and any device used for treatment and therapy must be provided with manufacturer instructions for decontamination which must include method, product for risk levels of contamination low, medium, high risk!. In the UK, decontamination is guided by medical devices directives and Health technical memorandum's on decon. There are also national standards for environmental cleanliness and infection control in the built environment guidance to refer to. Therefore plastic covering for floor and table is not needed as the environment should be appropriate to prevent infection and allow decontaminationalongside management and decontamination of equipment and medical devices.
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i need 15 minutes of the animal in anesthetic condition prescribed dose of  ketamine is -80 mg/kg and for xylazine 10 mg/kg, why we can not use either ketamine or xylazine,  plz let me know ?
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Follow the advice of Drs. Falsby and de Sagura.
The other people should read more and have more experience. Yet some ignorance is simply shocking. Why don't you talk to some anesthesiologist before speculating? Ketamine has been and is still used in war surgery as almost perfect anesthetic and analgesic. Muscle (thorax) rigidity is a rare and not well documented condition. Addition of sedatives diminishes dissociative effects (hallucinations and similar) and "may" relax muscles. In rat anesthesia this is of little relevance if you are not measuring respiratory parameters - and hardly anybody does it in rats because rat is not very good model for respiratory mechanics measurements anyway. However, ketamine has relatively short action and addition of other long agents may mask fading away of its analgesic effects - what is the most frequent mistake in animal anesthesia when ketamine is used!
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I am looking for software (free or paid) that allows monitoring data to be extracted from the GE Carescape B850 anesthetic monitor. Ideally the data should be downloadable in a CSV or Excel file.
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Monitor2 by James Derrick (Prince of Wales Hospital, Hong Kong) is available on the App Store (Free) for use on MacOS. Works well and produces nicely formatted charts but also can download data for further analysis in a spreadsheet or stats package.
The  VSCapture - from Sourceforge (a C# .NET program) is more basic but provides simple logging of data - I think as frequently as every 5s. The later requires  a framework such as Mono or  Xamarin to run in but once running is very simple and distraction free. Cross platform and should even run on Android though haven't tried this.
Both will need a mechanism to connect to the anaesthetic machine. The GE official sanctioned way requires the use of an ATEN UC-232A USB to serial adapter (connected to the 4th USB port), a null modem connector and a further serial to USB to get the data into the collecting device. (as https://www.researchgate.net/profile/John_Karippacheril identified above)
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Few patients with cardiac disease undergoing cardiac surgery(CABG, valve replacement...etc) develop atrial fibrillation with rapid ventricular response after induction.Some anaesthetists treat this arrhythmia others prefer not to ;especially if it is on pump surgery,any studies!
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Atrial fibrillation (AF) is common after cardiac surgery (33% of patients). Most cases are self-limiting (almost95% of case are free of AF at the time of hospital demission) . The rhythm control strategy (amiodarone and cardioversion) does not reduce neither the days of hospitalization nor the incidence of major complications, including death, stroke, or major bleeding.Nonetheless. rhythm control should be the first choice.
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In respiratory research a breathing apparatus consisting of mouthpiece, filter, Pneumotachometer, and non-rebreathing valves plus some connectors are usually used. Although a non-rebreathing valve is used to reduce dead space, each of these devices has its own dead space. Though small, adding together they build a relatively large dead space sometimes. What is the max acceptable dead space in a breathing apparatus, for a study including healthy adults?
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I fully agree with the first answer. I would however like to suggest using two pneumotachographs, one in the inspiratory limb, one in the expiratory limb. The sum of flow rates of both gives you the total flow rate. This way, the pneumotachographs do not contribute to dead space. You may consider this principle also for filters etc.
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I used to think that as Pcrit is the same during sedation and natural sleep, this means that the properties of the UA muscles remain intact under sedation, but then I read an old article that explained that because of the methodology to get the Pcrit, where the CPAP is on, the muscles don't have activity, and so you shouldn't expect to have a different Pcrit as, even if the drug would cause muscle relaxation, it would not make a difference in an already relaxed muscle....(Morrison DL, Launois SH, Isono S, Feroah TR, Whitelaw WA, Remmers JE. Pharyngeal narrowing and closing pressures in patients with obstructive sleep apnea.pdf. Am Rev Respir Dis. 1993;148:606–11.)
Now I'm reading an article by Eastwood about increasing dose of propofol and Pcrit and says that it increased Pcrit, so now I don't know what to think (Eastwood PR, Platt PR, Shepherd K, Maddison K, Hillman DR. Collapsibility of the upper airway at different concentrations of propofol anesthesia. Anesthesiology  2005;103(3):470–7.)
Can anyone explain me where's the problem? 
Thanks
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The side of OSA is the collapse of the upper airway during sleep, which raises CO2 and leads to increased ventilatory drive and increasingly negative pharyngeal pressure. These respiratory stimuli can activate the upper airway dilator muscles to restore pharyngeal patency during sleep, which can protect against OSA. However, restoration of sufficient airflow can only occur if ventilatory drive can build up during sleep without an arousal.  Instead, invasive procedures, such as an epiglottic or an esophageal pressure catheter, is required. Signals were sampled at 125-150 Hz data acquisition interface and displayed using software This method used to determine in each respiratory arousal threshold (Arth), could be used to measure the Pcrit.( Edwards, Eckert, McSharry, et al.: Predictors of the Arousal Threshold in Am J Respir Crit Care Med Vol 190, 11, pp 1293–1300, Dec 1, 2014)
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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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We're inducing repeated traumatic brain injuries in a closed-skull mouse model.
We chose isoflurane as the anesthetic because it doesn't have the neuro effects that injectables such as ketamine/xylazine do, and because it allows for quick recovery in order to be able to observe signs of TBI immediately.
It appears that after being anesthetized and impacted once (great recovery the first time), the mouse died during prep for the second impact. Isoflurane dosage was roughly the same as the first, successful impact, but the mouse died ~2-3 min after removal from gas chamber, at which point it was slightly under-anesthetized.
Is there a way to reduce the anesthesia dose while keeping the animal unconscious for the procedure? What differences in response to isoflurane would you expect in C57BL/6 mice? (the mouse above was BALB/c), and how would the mouse's age affect that prediction?
Thanks!
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How did you judge that the mouse was under-anesthetized? Under-anesthetized means  that the mouse seemed light in anesthesia?
Dying of anesthesia might be a "sign" of the first TBI; sounds stupid, but we are very concerned to anesthetize TBI (clinically) and therefore I would not exclude this option.
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sepsis spinal regional
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It is a very controversial topic. Infectious complications of the central nervous system (e.g., meningitis, epidural abscess, or others) following regional anesthesia on febrile / septic patients . In 2006, a well written paper by Dr. Horlocker from Mayo Clinic summarized the conflicting results of the studies that examined neurological complications in septic patients undergoing regional anesthesia (Link). Recently and to my best knowledge, my research group have a developed the first meta-analysis of individual participant data (in Peer review yet) on this topic. A total of 234 meningitis cases were found following regional anesthesia, 199 of them were related to spinal anesthesia, of which only 2 cases had previous bacteremia / septicemia. However, it is important to say that in 110 of the 199 cases had not a clear cause of infection (not reported).
In conclusion, actually, there is not a general consensus. As for the actual clinical practice on this topic, sepsis or bacteremia is not still a contraindicated condition for spinal neither epidural anesthesia. 
Of course, it is advised to follow an aseptic technique during the procedure and, from my perspective, wearing surgical masks because the droplets may be a potential source of infection according to our recent work.
Hope this help to answer your interesting question.
Regards
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My goal is to record EEG during anesthesia and analyse the row signal of EEG. So I am not considering devices using ready-made algorithms like BIS or others. 4-channel EEG will be enough, the main point is to obtain row signal! If there is no way to plug such a device an our monitor, we will probably go for a full classic EEG.
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Tim is correct. With a standalone BIS monitor, you can get two (but not four) channels, and these channels will be from the same side of the front of the head. To download via the BIS monitor you have to go into the settings and switch from ASCII to binary output, to enable downloading of the raw EEG via the RS232 port.
I too doubt that this is possible with a BIS module for use in other monitoring systems.
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In our hospital, we usually prepare endotracheal tube as immersing it into the sterile normal saline irrigation solution just before intubation in operation theatre.
I think that this maneuver helps to lubricate the endotracheal tube cuff to facilitate passage into the vocal cord and minimize dryness of throat and laryngeal injury.
I'm wondered whether this method is also used in other countries
How do you think about this? Please add your opinion or your routine maneuver.
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There is no need of any preparation, in our's institution's view. Just ensure proper relaxation before inserting the tube though the vocal cords. If the tube will be inserted though the nose, we lubricate it with sterile lidocaine gel.
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I wanted to get some information on the anesthetic management for an
adenotonsillectomy in a child suffering from PFAPA.
What attentions have in conducting / medication management?
You possibly references that I can point to?
Thank you in advance for your attention, friendliness
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Attempt to schedule when well (can be difficult). Continue medications I. E. Steroids or histamine antagonists.
Induction: Treat like they have OSA due to adenopathy and potentially crowded oropharynx, confer with surgeon. 
In all children (particularly syndromal kids) I keep things simple. SevofluraneN2o induction /fentanyl/propofol/ETT/paracetamol/ondansetron and good local anaesthesia by surgeon. There is no known link to malignant hyperthermia- and fever is a VERY late sign and should not be the factor that rtigers Rx. So I don't think that TIVA is required.
Post op: simple anslgesics. Oral oxycodone elixir as rescue if needed. Ideally monitor in HDU for 12 hrs if possible (I.E.  like OSA).
High risk of re bleed due to scaring- suggest to parent to stay within 1hr of Paeds capable facility for next 2 weeks.
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Dear Dr. Piccini and colleagues,
Many thanks for sending e a full text version of Paraesthesia after Local Anaesthetics: An Analysis of Reports to the FDA Adverse Event Reporting System. It is a very important work.
You may be interested in my continued research subsequent to my 2006 paper that you kindly referred in your article.
If you send me your e mail address, I would be more than happy to send you my recent works, a combined clinical- and registry study, and an animal experiment.
Kind regards
Søren Hillerup, PhD, Dr Odont.
Professor em., Maxillofacial Surgery
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I already had it, but thank you very much for thinking of sending it to me.
I understand you prefer not to give us your final opinion on Malet, Faure, Haas, and Lambert's work...And what about Stanley Malamed efforts to prove the inocuity of articaine in paresthesias ( he had a fierce opposition from Dr Haas - from Toronto)
But I would be very interested in your advice : may be by using my email address for privacy ? Or, is the question taboo?
Thierry
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Vitamin c 7 E has been implicated for analgesia.
Some recent advantages of pain relief with curcumin in mice have been reported.
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concerned vit. C, pre operative use to prevent CRPS was explored many times in the 2000's
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Extracorporeal shock wave lithotripsy accompanies with pain. Is it worthwhile to perform intercostal nerve block for pain relief during ESWL?
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NO
Regards
Prof Mo
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What's the most useful tool you rely upon to prevent yourself from making an error, ensuring that you've entertained all the important possibilities? Do you have a favorite saying or memory aid that you teach trainees? This could be for a specific condition (like the Hs and Ts of PEA) or a general approach to ensure you aren't missing something.
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Medical diagnosis is something more complicated than just to takeoff. Checklist are appropriate for repetitive situation requesting a stereotyped verification. Safe surgery checklist is a good example of it. You can find specialysed checklists addressing specific diagnostic situations: if you collect all of them, you'll have a big textbook in your pocket. A different approach is to focus on the situation leading to error and on the cognitive bias that can favorize errors. Mark Graber proposed a very simple checklist that can alarm you if you are in a situation at risk:  Graber ML, Sorensen AV, Biswas J, et al. Developing checklists to prevent diagnostic error in Emergency Room settings. Diagnosis 2014;1:223-31.
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I read lots of recent literature about this new technique. Would like to know more.
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For our facility: dieter.peuskens@zol.be
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I see many anesthesia techniques can be used for kidney transplantation.
In my hospital for recipient we use lower combined epidural & intravenous anesthesia (TCI propofol). Postoperative analgesia achieved by continous ropivacaine 0.15% + fentanyl 2 mcg/mL, rate 8 mL/hr via epidural catheter for 3 days and iv paracetamol.
For laparoscopic living donor we use combined epidural & general anesthesia (volatile). Postoperative analgesia: intermittent epidural bolus (bupivacaine 0.125%, morphine 2 mg, volume 10 mL, 2x/day) + iv paracetamol.
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For renal transplant recipients, we use Epidural Anesthesia and use fentanil with ropivacaine 0,2% In PCA post operatively. For donor, we use thoracic epidural in conjuction with GA.
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A Flow Trac gives a lot of information in managing a sick patient during surgery. What are your experiences? What group of patients do you usually use cardiac output monitoring on?
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I regularly use oesophageal Doppler in colorectal surgery. There is reasonable evidence indicating that outcomes are improved through improved fluid management. When an arterial line is indicated, I use a LiDCO monitor instead of the oesophageal Doppler (because it is faster & easier to set up).
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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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Dexmedetomidine is used as an adjuvant to intrathecal  local anesthetic                     (Bupivacaine/ Ropivacaine ). Does it help in prolonging duration of spinal anesthesia? How would you rate it on comparison to fentanyl/ morphine?
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Have never used it, coz this is the place where it can be carried to CNS and its vital tissues directly. However, in the epidural route and peripheral blocks the absorption characteristics are variable. But free accessibility of this drug to CNS structures while floating in CSF has not been studied extensively and mainly Indian studies are available only. Even the dose calculation is little weird when it is used intrathecally. Concerns from FDA are likely to come up soon regarding its intrathecal use.
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Hey , how are you doing today,
I did splenic injection of tumor cells with C57BL6 to accomplish liver metastasis.
,but I don't understand some results of my experiment,,
The main thing is that..
All mice woke up 1~2 hours after surgery, and they all looked fine.
However, 5 mice (among 48 mice) got weaker, and died 24~48 hours later.
I have checked bleeding, but no sign of bleeding was found.
Infection?, If it is about infection, is anti-biotic gonna be helpful?
Please give me some possible reasons for these deaths
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[Brief procedures]
1. Anethesia by using Ketamine/xylazine mixure (9:1).
2. the spleen was exteriorized via 5mm abdominal incision, and cell line was injected.
3. after 1 min (to allow cells to flow into the liver), splenectomy was done, and homoeostasis was assured by ligation with suture and pressure with a swab
4. suture.
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Thank you for your time and concern, :)
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have u checked the inflammation caused by the surgery itself?
the amount of cells inserted?
what we did was to pour iodine after suture, wrap the mice with gauze and place it in the cage.
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We have been using Ketamine + Xylazine as a standard anaesthetic for mice in our lab. However, due to some policy problems, ketamine is no longer produced here in China. I wonder if there is any other anaesthetic that have similar anaesthetic effect on mice? Please help me. Thanks a million!
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Hi, chloroform or ether is no longer used (depending on the countries) because they are too aversive for the animals.
It really depends what kind of procedures do you want to do to your mice. Isoflurane is good, but when the procedure induces pain, you should also give an analgesic as butorphanol or carprofen or fentanyl, as stated before. This procedure would be good for surgeries (don't forget post-operative care) since it provides a controlled level of anaesthesia in a long duration.  The limitation is that you have to have a vaporizer, which could be expensive.
For short-procedures when you give a bolus, I agree that you can use barbiturates as pentobarbital, with analgesia. As already stated you can use with barbiturates diazepam or medetomidine.
Propofol is a hypnotic, so you need analgesia and is quite good for surgeries when you can do an IV continuous infusion, however in mice it could be hard. You can also use  75/1/0.2 mg/kg of propofol, medetomidine and fentanyl, respectively, ip route, for short procedures and with a good analgesia (see paper attached).
Hope you can find a good solution for you and your animals.
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Recently we had a patient candidate for CABG who was alert and oriented. The first K after induction was 8 mEq/L. This number was confirmed by recheck. Two measurements on CPB were 6.5 (with low potassium cardiopledgia) and 7 (at the end of CPB). off pump K was 6.5 after giving insulin for BS=190 and NaHCO3 for acidosis (BE= -10). First postoperative K was 6.5 too. There was no EKG sign in perioperative period.
The patient had no Hx of renal problem with Cr=0.95 mg/dl. preop drug Hx included Aldacton 25 mg BD. however, last preop K was 4.8.
What's your opinion about this case?
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One may not find ecg change many a times. 
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In the analysis of research into the use of Citrate in the dialysis of ICU patients, there seems to be a positive swing towards the use of Citrate over other anticoagulants. With so many different types of modality being used with Citrate, Which mode seems to have the least complications? All suggestions welcome.
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CVVH is the simplest and most efficient system. Adding dialysate does not increase efficiency as many believe! And if you have pre-dilution, that reduces efficiency as well. CVVH also makes calculations easier and is predictable!
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With the shortage of funds within the health service, can we really turn to SLED or SLEDD as an alternative to continuous renal replacement therapies?
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Your question implies that there may be increased cost of SLED, compared to CVVHD/CVVHDF. This is not necessarily true. Costs will vary according the the number of patients (economies of scale) and the availability of equipment and trained staff.
For SLED, the cost of equipment is high. The equipment is more complex and more staff training is required. SLED typically (but not always) generates the dialysis fluid online from a pure water supply and liquid concentrates and dry powder. SLED can use the same equipment and trained staff as used for standard chronic dialysis. SLED typically runs for part of the day only (not continuous)
CVVHD or CVVHDF use a simpler machine running continuously. It requires approximately 50 litres per day of special bagged sterile fluid, which is expensive and creates logistical problems.
For a hospital which has facilities for dialysing patients with chronic renal failure, and only occasionally need to provide dialysis in ITU, SLEDD will be much cheaper than CVVHD. In this case, appropriately trained staff and equipment are already available in the chronic dialysis unit and could be transferred to the ITU when required. SLEDD may avoid the cost of the sterile bagged fluids.
For  a hospital which regularly dialyses patients in ITU and does not have a chronic dialysis facility, CVVHD may be cheaper. In this case, the ITU staff will acquire and maintain the appropriate skills and equipment. The cost of the dedicated CVVHD equipment, logistical infrastructure and training will be shared between many ITU patients. 
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It is often seen that patient complaints of chest pain, either in left side or in epigastrium, during cesarean section under spinal anesthesia. It specially seen during peritoneum stretching, uterus manipulation or rough handling of omentum etc. What is the probable cause and what should be the ideal prophylactic and therapeutic strategy?
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Though chest pain during cesarean section under spinal anesthesia is a common entity, the cause is still obscure and there are several hypothesis. Myocardial ischemia from oxytocin may cause chest pain but this is definitely not a common finding. High thoracic block and inadequate block height are not also the most common reason as there will be other obvious signs.
Hypotension may cause chest pain and it is common after abdominal delivery of the fetus due to hypovolemia, but the more obvious sign will be nausea and vomiting caused by decreased blood supply to chemoreceptor trigger zone (CTZ).
In my personal opinion, the most common cause of chest pain is probably due to peritoneum stretching leading to vagal stimulation. It is specially seen during peritoneal closure (some surgeons still do), uterus manipulation or rough handling of omentum etc. If unattended it can lead to bradycardia and even cardiac arrest. The most effective management is reassurance, sedation and atropine in vagolytic doses.
Again, chest pain under spinal anesthesia is not only unique to C-section, it is also seen during appendicectomy under spinal anesthesia, specially in male appendix probably due to anatomical variability. That is why GA is safer option during appendicectomy,  at least theoretically.
Another explanation of chest pain is microembolism. When uterus is exteriorised and placed above abdomen, microembolism can occur due to concomitant hypotension (hypovolemia following abdominal delivery of fetus) and air entry into microvasculature. This microemboli can lodge in pulmonary circulation leading to chest pain. In support of this theory lies the fact that chest pain is seen in mainly those cases where uterus is exteriorised and placed above abdomen. If surgeons manipulate uterus within abdominal cavity, then the incidence of chest pain is very less. Some anesthesiologists like to administer prophylactic vasopressor beforehand to raise the BP and diminish the chance of microembolism and this technique do actually work!
It is fact that microembolism is definitely a cause for chest pain but this can not explain the occurrence of chest pain during appendicectomy under spinal anesthesia.
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Position plays a vital role in subarachnoid blockade specially while using hyperbaric local anesthetic agents. Sitting or supine position may affect the final height of the block. Is there any modification of positioning while using isobaric local anesthetic agents?
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Contrary to hypo- and hyperbaric solutions, a true isobaric solution does not exist. This has to do with the variation in the density of c.s.f. between individuals. Hyperbaric solutions are defined as having a density > 1.0015, and these solutions will be hyperbaric in all individuals. Hypobaric solutions are defined as having a density < 0.9990, and these solutions will be hypobaric in all individuals as well. The traditional definition of an isobaric solution is a solution with a density between 0.9990 and 1.0015, but it is obvious that a solution with a density of, say, 0,9992 will be hypobaric in an individual with a c.s.f. density of, say, 1.0012. Conversely, a solution with a density of 1.0012 will be hyperbaric in an individual with a c.s.f. density of 0.9993. Another complicating factor is that the density of a solution is inversely related to temperature. Since local anesthetics are usually injected at room temperature, the density of that solution will decrease during equilibration to body temperature. With a true hypo- or hypobaric solution this change in density will not have much impact, but with a solution that has a density in the range of 0.9990 - 1.0015 the change in density may also cause a change in baricity. This has been amply demonstrated with plain bupivacaine, a solution considered to be isobaric: When plain bupivacaine is stored in a refrigerator an injected with a temperature of 6 degrees Celsius, the solution shows a hyperbaric distribution pattern. When the solution is warmed to body temperature immediately prior to injection, it shows a clearly hypobaric distribution pattern.
Is there nothing to say then about position and "isobaric" solutions? Yes there is. Plain bupivacaine is slightly hyperbaric at room temperature, but hypobaric at body temperature. During thermal equilibration, which will take an assumed 1-2 minutes, the baricity of the solution changes. This is best demonstrated by the following: When injecting plain bupivacaine in the lateral decubitus position, the maximum level of sensory blockade is unpredictable and may vary from very low to high, making this technique only reliable for lower limb surgery. However, injecting plain bupivacaine in the sitting position and maintaining this position for 2 minutes will usually result in a maximum level of sensory blockade above the tenth thoracic dermatome.
An important thing to remember: Position may be used as a tool to affect the maximum level of sensory block, but it is not suitable for accurate "steering" of the maximum level. Postion mainly affects the initial spread during the first minutes. It usually takes 10-15 min to determine if the maximum level of sensory block is going to be adequate, too high or too low; at that time, changes in position will have a minimal or no additional effect on the maximum level, asuming that a normal dose of local anesthetic has been used.
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We use controlled breathing with LMA quite often. Some of my patients complain of stomachache following the surgery. Although appropriate sealing is achieved, it occurs to me that it could be due to air insufflation through LMA. What do you think? Any similar experiences?
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Who is not recommending? It is no problem at all, provided that the patient has an empty stomach. There is no need to struggle with an ETT for the sole purpose of controlled ventilation, when you can just as easily insert an LMA.
A properly inserted LMA sustains a 20cm H2O pressure gradient, sufficient for most patients. We routinely use LMA´s for malignantly obese (BMI>50) patients in ramp postition.
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This is quite bold but I am currently looking for a job. Since my degree will be in medicine I would very much like to get into patient care. Nevertheless I'm very fond of research and particularly psyched by systems biology, quantitative biology and emergent behavior in dynamic open systems since I did my pre-clinical studies.
My current problem is that I'm not quite sure where to turn to if I would like to pursue my scientific interests. I'm not bound to any specific discipline, but anesthesiology, internal medicine and neurology are my favorites at the moment.
Are there any hospitals participating in systems biology research in Europe? I was looking into it and found that Charité Berlin is the only hospital displaying their involvement.
I would be really grateful for some advice!
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A brilliant question. How I wish I had ResearchGate to ask this in 1970.
My first thought would be to follow my father's advice - looking after patients is the most rewarding thing and keeps you sane while the research is slow. Doing both is hard but perfectly possible and I would not have wanted to miss out on either. Moreover, looking after patients shows you what the real problems are - the ones worth spending twenty five years on.
Doing clinical work and research together successfully has always been a question of breaking the rules. If you follow the rules you will be stuck in treacle. Taking your own path can be lonely and frightening at times but you have to stick to the motto of the Royal Society 'Nullis in verba' - never believe what someone else says. So there is no way to advise on 'which department to work for' or 'which area to target'.
Which brings me to the next point which is my advice to find your very own question to ask and answer. Forget what everyone else is asking, find your own question. If you cannot think of your own question then you have to wonder if you are suited to research. (Unfortunately research is full of people who cannot think of their own question.) And be prepared to keep asking one question for thirty years. What you should not do is stick to the same answer for thirty years - that is the sign of failure. Wisdom is discovering you were wrong, and wrong again, and again.
Now for the knock-out point. Forget systems biology and emergent behaviour. Systems biology is just a meaningless fad. It is bad science. The body has no systems. Everything dovetails with everything. The protein that lubricates joints comes from the same gene as megakaryocyte stimulating factor. As my hero Leibniz pointed out there are no systems in nature. The current fashion for systems thinking is a march back into the middle ages. It imposes presuppositions that stop you thinking. And I have no idea what emergent behaviour is really supposed to be but I am fairly sure it does not exist in complex dynamic patterns with parts. The idea is used by people to bullshit mostly - to give the impression you have an explanation when you do not. Something like emergence does appear in terms of the partless units of quantum field theory but that is another story.
So in summary my advice is to find your own question - based on talking to people with illness. I found my question talking to people with rheumatoid arthritis. You might find it with Parkinsonism or multiple sclerosis - both well worth a lifetime's effort. And learn to forget fads like systems biology. They have nothing to do with productive research.
The biggest and most interesting problem of all is how we come to have thoughts. And why thoughts go wrong in schizophrenia is perhaps the most worthy question. Mental illness is worse than hell for the sufferer and their family. I am too old to solve this one but you might look at http://www.ucl.ac.uk/jonathan-edwards if you are brave enough to break some rules and think some different thoughts!!
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What is your opinion regarding a request for epidural labor analgesia for a parturient woman with fever (38 º Celsius) and leukocytosis plus neutrophilia and no focal infectious signs? Would you use it or refuse?
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We routinely place epidurals in such patients after they have received intravenous antibiotics. It is important to find the source of the infection. In our laboring patients, we find that chorioamnionitis is one of the major source of infection and subsequent fever.
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I've just started recording evoked potentials in mouse neocortical brain slices, using a constant voltage stimulus (0.1Hz at approx 1V). I see that most people use constant current generators for this purpose. Is a constant current stimulus essential to ensure stable responses over 1-2 hours?
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It is desirable to use constant current and not constant voltage for the stimulation. The impedance (resistance) of the tissue is changing due to some electrochemical processes (polarization, oxydation/reduction). Thus, in constant voltage stimulation, the current delivered to the tissue will be dependent on the resistance of the electrodes and the tissue, simply by the Ohm's law. However, in the case of constant current stimulation, the changes in resistance of the electrode/tissue will have a little effect on the delivered current. Again, according to the Ohm's law, the resistance could increase significantly and diminish the current injected to the tissue. However, one can keep the current constant, and overcome the changes in resistance by adjusting the voltage. Obviously, there is a limit of how much we can increase the voltage to overcome the resistance changes >> stimulation compliance. Most constant current stimulators have a compliance of tens to hundreds of volts.
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I was attempting to anesthetize the animal with diazepam and ketamine, the pup vocalized throughout the surgical procedure (removal of dermoid).
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Aswathy, good to know it wasn't that much atropine... Still a fairly high dose, which might have caused trouble as it could have been enough to cause excitement in a puppy. As for the lidocaine, I know the literature, but being a veterinary anesthesiologist who has done a lot of patients, I can tell you confidently that these numbers are a bit high in real life cases. Studies typically don't take other drugs into account, age, breed specifics etc.
Anyway, question is, why was your puppy not acceptably anesthetized with technically enough anesthetic given?
Would be interesting to do the same with proper sedation, but of course, we cannot go back in time. While benzodiazepines work great in humans and typically in true neonates (all species), once they grow out of the first weeks in age benzos are not very reliable in dogs (and even worse in cats, and terrible in horses). If we assume the benzodiazepine didn't do its job in this case here, we can look at ketamine as a single agent to produce anesthesia. Because it is a dissociative the signs you observed might be than not too surprising. You probably still had muscle relaxation due to the diazepam, but not the calming effect. I don't think the pup was in pain considering all you gave and if your local block (what exactly did you do?) worked.
Interesting case. Thanks for sharing.
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I work at two centers with different approaches. Thank you for your response.
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Dear colleague
In clinics where I worked, iNO is used in closed circuit, without the need to exclude lime soda or to modify the intake of volatiles. On the other hand, I observed increasingly tend to use more intravenous hypnotic agents than inhaled, but not because of interaction with iNO. If you have the experience to shift from iNO administration to ECMO in OR, it must be more careful to avoid volatil anesthetic, because they interact with materials of ECMO oxygenator.
An other approach is in ICU, were ventilation machine are with open circuit. iNO can be connected directly to Y-piece, and adjust their concentration depending of minute volume.
I hope my answer will be useful for you.
Greetings from Moldova.
Dr. Veaceslav SAVAN
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Dobutamine is considered as the first line inotrope for perioperative hemodynamic support in cardiac surgery by some of the classic references. What is your inotrope of choice? Have you stopped dobutamine due to adverse effects?
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Well well well -
the point is what do I need the drug for......
1. if i have anesthetic side effects - low BP due to Propofol etc - and the rest of the heart is fine - NA is the drug of choice.
2. if I have low CO and adequate BP - the point is to increase CO with inotropic support and afterload reduction - dobutamine, milrinone, enoximoen etc are fine - and studies exist
3. if there is severe impaired CO - the use of adrenaline together with afterload reduction (i.e. milrinone, phenoxybenzamine, phentolamine, etc.) is the combination of choice - may be as an add-on to the things mentioned above
4. if there is low BP - needed for organ perfusion - some NA may be helpful if dobutamine lowers the BP too much
5. dopamine - especially low dose - is useless and only increases afterload and shows a good BP, only increases the rate of sepsis, impairs endocrine function, has no effect on kidney function, etc, etc,
here you are - open for discussion
Nik
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We use tried and tested methods in evaluating a trainee's academic progress but what of progress in terms of apprenticeship for the profession? I suspect most of us use a subjective/semi objective method of assessment based upon observation of the trainee's practical abilities in the OR, but to what extent is that progress identifiably due to interaction with a senior during supervised sessions, or due to the individual effort of the trainee? I suspect that it's a bit of both and that the balance alters during training, but is there any way of identifying each component? Can we identify the point at which a trainee is capable of the (often subconscious) complex situational analysis required of a specialist anaesthesiologist? Also, is there ever a point in a trainee's progress at which the presence of a senior in theatre becomes a hindrance rather than a help to further progress?
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Recent common practice is to evaluate residents or trainees at different levels, by different providers and through different tools. I think a combination of a socratic approach (test what you know) combined with a experienced based (kind of aristotelic). We often assume only to know and that where both faculty and trainees failed to approach truth. Practical abilities cannot disconnect from formal knowledge, besides, very skillfull person do not necessarily have the body of knowledge regarding a topic. They still happen to know and do it fast and correctly (observation, imitation, repetition, in a word ACCURACY and PRECISION?).
The introduction of simulation and evaluations of trainees by different providers are objective measures fo an otherwise difficult assessment. However, in a honest and well educated manner, we all know the trainees that are capable from those that barely are functional. In general we assume that anyone can do it, and in fact is very rare someone will be incapable. As well as few will be exceptional, but in general with proper training, but also POST training experience and self evaluation, we all reach the flat side of the curve. I agree that levels of different training requires different levels of self constructed situational experience, meaning, you have to do yourself. The senior specialist in that case could be an obstruction depending on 2 factors: the eagerness of the trainees to refer for advise (capacity of LISTENING), the interference of the faculty by intervening when not necessary (capacity of observing). But can the trainee also practice on his/her own license?
I personally think that a system like with multiple levels of trainees accountability (british?), junior, senior, pre-consultant, offers a good model. In many other countries this is replaced by fellowships or other types of postgraduate training. Even in the best programs where you are exposed to several procedures and activity, the difference between capable to do it, and really experienced to do it, that encompasses not only the skills but the ability of the situational awareness makes the difference. I do think we are making effort to educate about being actually a mature professional anesthesiologists, my only hope is that any attempt to reduce training lenght (justified by some by the smarter "kids") would be discouraged, while restructuring training to further develop the "wise" people we need.
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The course is directed for nursing students specializing in anesthesia.
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You can refer some books like...
Rang & Dale (to study the pharmacological effects as well as specific adverse effects of individual anaesthetic agent)
Stages of General anaesthesia is well given Goyal RK as well as also given in Rang & Dale.
You can also refer KD Tripathi for preferable dosage of General anaesthetics.
Otherwise as Abusalemsir have suggested, refer Lippincott (a reference book) for other details regarding GA...
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After CSE for labor, cesarean section performed in epidural and post operative analgesia without any problem, after catheter's removal we assisted to important spillage of cerebrospinal fluid for a lot of hours.
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We too have hoped it. But it was really CSF fluid: specific tests have confirmed it!
without a shadow of doubt!!!
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What is your practice, recommendations, and experience in optimizing preoperative Hb? When do you give Iron and Erythropoietin? Which one is superior? Any other alternatives to minimize perioperative blood transfusion?
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Dear José,
I fully agree with your assessment of oral iron having a longer latency, but in Germany, iv iron has a restricted indication. I also agree with your statement about iv iron beeing safe, but again, this is not translated in a broader indication for iv iron. Most preparations can only be used, when oral iron has shown no or not an adequate effect or intolerable side effects. Only currently, the indications of iv iron broaden.
As to the time until surgery, this is the reason, why GPs and other colleagues have to be included into a PBM program: Elective surgical patients shouldn´t be sent to the hospital only one or a few days before surgery, but at least four weeks in advance to assess preoperative anaemia. Urgent or emergency surgery of course has to be performed without delay and without without further dealing with anaemia other than RBC transfusion if necessary in the individual situation.
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I am performing in vivo electrophysiology on Sprague-Dawley rats, recording local field potentials and spiking activity in the VTA, SN and PFC.
I have narrowed my choices down to Chloral hydrate, Isoflurane and Urethane. Aside from differences in route of administration, are there any real advantages of one over the other? Is there a better anesthetic agent apart from these three I mentioned?
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From your description of your research and the recorded regions I imagine you are at least partially interested in synchronization/coherence between oscillatory signals in the dopaminergic midbrain and the PFC. If that is true, you should probably use urethane or chloral hydrate, since with these anesthetics you preserve the spontaneous slow oscillations (up/down states) in cortex and VTA. If spontaneous oscillations are not that important for your research question, then isofluorane would probably be best, as it allows for very quick induction and recovery and fine control of anesthesia depth, even though it suppresses burst activity in the cortex.
These papers might be useful for you:
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Hypothesis: Anesthesiologists are experts in resuscitation and crisis management, and if present at the scene of illness or injury and transport of selected critical patients, this will improve survival and reduce long term disability.
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I think it is a fundamental error to assume that any one group is best at prehospital care, however I also think that the arguments in this area are often well rehearsed but usually miss the point. There is no intrinsic need for paramedics, for instance, to be trained to intubate, rather than to use an LMA for instance, particuarly in the context of the availability of devices such as the iGel or the King airway. The skill of endotracheal intubation may or may not be necessary for a particular group of patients, with a particular pathology, but most of the discussion seems to centre around what people feel SHOULD be part of their skill set.
A classic example of this is in cardiac arrest; the evidence gathered and reviewed for the 2010 ILCOR guidelines showed no evidence of benefit for ETI in out-of-hospital cardiac arrest patients. What HAS been demonstrated is that there is definite harm in over ventilation, which is common and particularly exacerbated when there is a closed circuit as in the presence of ET intubation, and that in fact there is no survival advantage in anything beyond bag, valve, mask ventilation. Why then should there be a need for a wholesale training in ETI, with the concomitant training and skill maintenance burden. In large ambulance services such as exist in Australia, paramedics are estimated to perform an ETI about once a year. This level of frequency is almost certainly going to lead to poor performance.
Similarly, anaesthetists (anesthesiologists) are a variable variable bunch, some of whom, as pointed out by Eric Lawes, may have limited current familiarity with crisis management. In the UK, where I trained in surgery then emergency medicine, we often had the ridiculous situation of senior ED doctors who had long airway management experience, particularly in the prehospital setting, having to wait in the resus room for a junior anaesthetic person to come to assess a critically ill patient, just because "anaesthestists manage airways'. In Australia where I have worked for over a decade, emergency physicians routinely manage all airways up to the point of rapid sequence induction / difficult airways, and anaesthetists are almost never seen in ED. The concomitant result of this is that anaesthetic trainees almost never see the sort of dirty airway that we do (drunk, agitated, trauma etc) and are therefore not very well trained in it.
The point overall though, is that patient need should drive all of these arguments. In the prehospital setting, what should be considered is exactly which intervention is NEEDED by the patients given their clinical condition, and if ETI is necessary for a substantial proportion, consideration should then be given to how this is best achieved. With increasing education and recognition of issues such as patient deterioration, hypoventilation, poor perfusion etc, by paramedics, and the increasing prehospital availability of devices that can deliver NIV for example, the actual need for ETI is very small indeed. In this context, solutions such as having a rapid response scheme taking ED physicians, anaesthetists, or whoever is best and most experienced at the job, to the patient in the right time frame makes a lot more sense.
In NSW, we have a medical retrieval service that responds to critical care level interhospital retrievals, but also a substantial proportion of primary trauma and rescue scenes. The helicopters are staffed by a mix of ED / anaesthetic / ICU doctors, all of whom perform the same function, and who work with Special Casualty Access Team paramedics on all jobs. This system works extremely well, if for no other reason because the patient need and requirements for intervention are what drives the use of the system, not because the clinicians happen to be there and want to intervene.
The smartest clinicians, from paramedics to nurses to doctors, recognise the need to prevent interventions such as ETI, rather than perform them. Crisis management is the real skill, and this can be owned by clinicians of any background.
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Any reference for anesthesia management of such a complicated operation
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Hi
epidural, awake arterial line, gentle induction, cvp line, big drips
use diamorphine 2.5-3mg diluted in saline down the epidural without local anaesthetics. This will provide hemodynamic stability during surgery
I normally use remifentanil infusion for intraoperative analgesia. This is better than using local anaesthetics in the epidural because the sympathetic blockade due to epidural complicates our hemodynamic management.
I use Nor-adrenaline infusion and GTN infusion to manage the clamping and unclamping hemodynamic changes. Use cell saver during the surgery. If your patient is on dialysis he would be hypovolemic. you need to take account of it. other things like temparature, urinary catheter (if passing some urine) are routine
once the main procedure is over and unclamping of the aorta is done and you are happy with volume status of the patient load the epidural with bupivacaine. Extubate awake. cross match blood and book ITU bed for post -op. If you have access to cardiac output monitor and BIS those would be very useful
Hopefully it goes well
Balaji
Anaesthetic consultant
UK
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Do you use difficult airways algorithms and guidelines in your daily practice or do you have your own strategy? Which algorithm have you found preferable? Do you think current guidelines are simple and easy? Any recent updates?
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ASA published only recently their updated airway algorithm (Anesthesiology 2013; 118:251-70). Current algorithms (ASA, DAS) are very useful, but we found some of them difficult to follow in critical airway situations. We developed our own algorithm which starts with mask ventilation - the first measure the anesthesiologist will try if any problem occurs. We also included all the tools that are available at our institution. I attached a translated version of the algorithm. Any critics? Suggestions?
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The use of levosimendan is discussed in some interesting papers published recently. Unfortunately, data on pediatric and neonatal populations remain weak. Moreover, even if pharmacokinetic studies exist, the exact dose scheme and timing for administration were not clearly established in this population. Do you administer a loading dose? Do you consider the administration of levosimendan at the end of cardiopulmonary bypass, just before surgery, the night before ? Does levosimendan decrease the total amount of vasoactive agents administered? Does levosimendan improve outcomes, ICU length of stay, morbidity, and mortality? I think that it would be interesting to start levosimendan infusion at least 12 hours before surgery. Would be interested to receive informations about your experience.
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Use of Levosimendan in a pediatric patient with dilated cardiomyopathy is very usefull !!!. We use Levosimendan instead of a continous inotropic support in all pts with DCM and CHD in the pediatric group (from newborn to adulthood).