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Questions related to Critical Care Medicine
What are the primary challenges in implementing standardized pediatric care norms in resource-limited settings,
Multi-Organ Dysfunction Syndrome (MODS) refers to the progressive dysfunction of two or more organ systems as a result of an acute illness or injury. It is a severe and often life-threatening condition that occurs in critically ill patients. MODS typically develops in response to a systemic inflammatory response triggered by conditions such as sepsis, severe trauma, major surgery, or other critical illnesses.
The primary goals of critical care medicine revolve around providing comprehensive care to patients with life-threatening illnesses or injuries in the intensive care unit (ICU).
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?
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?
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
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?
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?
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?
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?
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
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)?
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).
Whether we use in operating rooms or in intensive care for various reasons and with acceptable cuff pressures
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.
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
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
Is there a positive effect on parallel canullamanegement and the weaning of ventilation? Or is there to less evidence of effectiveness?
Ivabradine, beta blockers, negative inotropic effect, HOCM, research paper
Risk factors for CRBSI are well documented but I´m looking for a sort of screening tool in ICU pacientes with CVC.
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??
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?
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?
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?
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?
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?
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.
my patient is 24 years old person , he has tracheal stenosis and stem bronchus stenosis , could it be tracheal hamartomas ?
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
Ultrasound has been used for different functions, what is its role in the diagnosis, evaluation and evolution of intra-abdominal hypertension?
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
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.
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.
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.
NOACs anticoagulant treatment
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
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?
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?
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
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?
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?
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?
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.
Trying to gather resources for standardized or widely accepted assessments used in the rehabilitation portion of burn care.
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
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.
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?
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?
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?
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?
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.
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)?
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!
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.
Is there a correlation between the number of days premature infant required mechanical ventilation increase chance of requiring or needing bronchodilator therapy?
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.
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.
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?
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?
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?
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?
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?
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?
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?
In critically ill patients, they may show some endocrine dysfunction. Waht test is useful in these patients?
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 ...
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.
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?
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?
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.
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?
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.
Dual modes of ventilation seem to be more physiological.
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.