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Reviews and Summaries

Mind the GAPS Study - Compression Stockings are Useless for Most Elective Surgery Patients!

14/9/2020

 
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Cricoid pressure prevents aspirations, preoperative antibiotics avoid infections, and compression stockings protect against deep vein thrombosis.  Many medical measures aim to reduce morbidity and mortality among patients, but unfortunately, the benefit of these measures is often not, or insufficiently, proven. Under certain circumstances, they may lead to additional problems or even cause harm (e.g. cricoid pressure Read Here).

Time has definitely come to take a closer look at compression stockings for surgical patients. Apart from the fact that they look terrible, they are just as uncomfortable to wear and even carry certain risks in patients with peripheral vascular disease, for example. The effectiveness of compression stockings in modern practice has been questioned, but robust evidence has been lacking.

This seems to change, as the long-awaited GAPS-Trial has been published and now provides further evidence on what concern patients undergoing elective surgery. 
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​Among this population, adding compression stockings to pharmaco-thromboprophylaxis was non-superior compared to pharmaco-thromboprophylaxis alone (primary outcome). There was also no difference in the quality of life outcomes found (secondary outcome).

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There is now some robust evidence to omit compression stockings in surgical patients that receive pharmacological thromboprophylaxis.


Shalhou J. et al. BMJ 2020;369:m1309

​

Antibiotics - Again Less Seems More - This Time: Uncomplicated Diverticulitis

3/9/2020

 
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The W.H.O. has repeatedly warned that antibiotic resistance is one of the biggest threats to global health today. Among all measures we can take to try and reduce this problem, merely avoiding unnecessary treatments is maybe one of the most effective. 

It is therefore pleasing that another piece of good evidence has been published, supporting the avoidance of antibiotics in the event of non-complicated diverticulitis (defined as non-perforated diverticulitis with a Hinchey 1a grade in computed tomography).
The investigators performed a 

randomized, placebo-controlled, double-blind trial 

in which they compared 180 patients with non-complicated diverticulitis

to receive

either cefuroxime, metronidazole, and amoxicillin/clavulanic acid or placebo.

They found

No significant difference in the median time of hospital stay (primary outcome). Also, there were no significant differences between groups in adverse events, readmission to the hospital within one week, and readmission to the hospital within 30 days.
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These findings complement other studies indicating that observational treatment without antibiotics can be considered appropriate in patients with uncomplicated diverticulitis.

​Clin Gastroenterol Hepatol. 2020 Mar 30;S1542-3565(20)30426-2

More literature

Daniels L et al. BJS:  https://doi.org/10.1002/bjs.10309

Int J Colorectal Dis. 2015 Sep;30(9):1229-34.

ARDS in COVID-19: Is it Time to Let Go of the High-PEEP Strategy?

31/3/2020

 
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​The lastest updated surviving sepsis guidelines for COVID-19 patient recommends a high-peep strategy in the intubated, mechanically ventilated patient. As most of these patients present with moderate to severe ARDS, PEEP is used to keep lung areas open and therefor to improve oxygenation. This seems to be especially true in the classical case of ARDS, where the lung become 'wet' and 'heavy' which results in widespread atelectasis of the dependent parts of the lungs, often further complicated by pleural effusions. 

Classical CT appearance in the acute phase of ARDS is an opacification with an antero-posterior density gradient.  Dense consolidation in the most dependent regions merges into a background of widespread ground-glass attenuation and the normal or hyperexpanded lung in the non-dependent areas (Howling SJ et al. Clin Radiol 1998;53(2):105-109). The theory behind these changes is that the increased weight of overlying lung causes compression-atelectasis posteriorly. The fact that prone positioning these patients quickly redistributes these gradients supports this theory (Desai SR et al. Anaesthesiology 1991;74(1):15-23).
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Classical ARDS finding in pneumococcal pneumonia

​Chest CT's in patients with COVID-19 often show ground-glass opacification with or without consolidations. These are changes often seen in viral pneumonia. Several case series suggest, that CT abnormalities seem to be mostly bilateral and tend to have a peripheral distribution, often involving the lower lobes. In contrast to the classical ARDS pleural thickening, pleural effusion and lymphadenopathy seem to be a less common finding (Shi H et al. Lancet Infect Dis 2020).
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ARDS in COVID-19 patient

The leading problem in COVID-19 patients with ARDS is hypoxemia, while hypercapnia does not seem to be a significant problem. Sometimes profound hypoxemia does not seem to correlate with patient symptoms at all. In regards to the images above, atelectasis might not be the predominant reason for V/Q mismatches in these patients. 

Observations of mechanically ventilated patients in our unit and other hospitals in Switzerland have shown, that higher PEEP levels (15cmH2O and higher) often result in significantly reduced compliance values complicating ventilation and favouring the development of pulmonary over-inflation. This observation might support the theory that patients with COVID do not represent the traditional manner of ARDS with distinctive atelectasis. Another observation that supports this theory is that COVID-19 patients often do not respond as clearly to Prone Positioning as classical ARDS patients do.

More probably, V/Q mismatch seems so happen on a more microscopical level in COVID-Patients. Lung compliance is often normal on these patients and, therefore, applying high PEEP-levels does NOT add any benefit at all.

Maybe the principle of less is more also applies to COVID-19 patients we treat (Gattinoni L et al. Intensive Care Medicine; 46, pages780–782(2020))


Looking at the New Surviving Sepsis Campain COVID-19 Guidelines:
Given these considerations, the strategy with High PEEP-levels in general should be questioned in principle.

@ILCOR 2020: Let's Put the Supraglottic Airway First!

13/2/2020

 
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​The International Liaison Committee on Resuscitation has published the last guidelines for advanced cardiac life support (ACLS) on resuscitation ILCOR in 2015. Usually, these statements are updated every five years, but 'Circulation' has now published an AHA (American Heart Association) focused update due to an increased number of studies looking at ACLS-specific interventions.


These updates are focused on three specific areas:
  1. Advanced airway management
  2. Vasopressors
  3. Extracorporeal cardiopulmonary resuscitation ECPR


​No News in regards to Vasopressors and ECPR

Vasopressors in Cardiac Arrest


  • Epinephrine (aka Adrenaline) should be administered to patients with cardiac arrest (Class I; Level of Evidence B-R)
  • It is reasonable to administer 1mg every 3 to 5 minutes (Class IIa; Level of Evidence C-LD)
  • High-dose epinephrine is not recommended for routine use in cardiac arrest

The bottom line:​ Great, these recommendations are no real news and do not change current guidelines at all.


Extracorporeal Cardiopulmonary Resucitation ECPR

  • There is insufficient evidence to recommend the routine use of ECPR for patients with cardiac arrest AND ECPR may be considered for selected patients as rescue therapy when conventional CPR efforts are failing in settings in which it can be expeditiously implemented and supported by skilled providers

The bottom line: ECPR is not for on the roads and remains an exception in general.



Advanced Airway Management

Taking recent evidence into account the updated guidelines 2019 conclude:
​
  • Either BMV or an advanced airway strategy may be considered during CPR for adult cardiac arrest in any setting (Class 2b; Level of Evidence B-R).
  • If an advanced airway is used, the SGA can be used for adults with OHCA in settings with low tracheal intubation success rate or minimal training opportunities for ETT placement (Class 2a; Level of Evidence B-R).
  • If an advanced airway is used, either the SGA or ETT can be used for adults with OHCA in settings with high tracheal intubation success rates or optimal training opportunities for ETT placement (Class 2a; Level of Evidence B-R).
  • If an advanced airway is used in the in-hospital setting by expert providers trained in these procedures, either the SGA or ETT can be used (Class 2a; Level of Evidence B-R).
  • Frequent experience or frequent retraining is recommended for providers who perform ETI (Class 1; Level of Evidence B-NR).
  • Emergency medical services systems that perform prehospital intubation should provide a program of ongoing quality improvement to minimize complications and to track overall SGA and ETT placement success rates (Class 1; Level of Evidence C-EO).​
​

We Suggest: Put the Supraglottic Airway First!


​In regards to these updated guidelines, the necessity of optimal cardiopulmonary resuscitation (CPR) during resuscitation and practical considerations, it seems reasonable to put the supraglottic airway (SGA) to the very top of airway management!
​Here is why:


  • During resuscitation maintaining circulation and therefore vital coronary perfusion pressure (CPP) is the mainstay of success
  • BMV requires interruptions of CRP (30:2),  this is deleterious!
  • Avoiding unnecessary interruption of compressions remains therefor a top priority. Interruptions result in the sudden collapse of CPP, which will hinder successful CPR ​​
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Avoiding interruptions is the key to successful CRP and therefore survival
​
  • Bag mask ventilation (BMV) can be quite tricky, especially when performed by untrained personnel. 
  • BMV is NOT a secure airway; the risk of aspiration is significant!

On the other hand

  • While providing a 'secure' airway, successful endotracheal intubation requires skilled hands and regular training
  • ETI's are mostly outside the scope of practice among many doctors, nursing staff or paramedics
  • Intubations under CPR conditions are never easy and might be even more challenging out-of-hospital
  • Again, CPR is often interrupted to provide optimal conditions for endotracheal intubation

It, therefore, seems plausible to put the supraglottic airway first. Not only first as a choice of airway management, but also one of the first things to do:

  • Placing a supraglottic airway (SGA) is simple and straight forward. Anyone can learn this procedure in a short time. We teach ICU doctors and nurses successfully on how to use non-inflatable supraglottic airways (e.g. the i-Gel device) for CPR.
  • Placing an SGA is easier than simple bag-mask ventilation (BMV)!
  • An SGA allows continuous compressions and ventilation simultaneously - no need for deleterious interruptions
  • An SGA protects the airway from aspiration fairly well - some devices even allow the introduction of a small suction catheter into the stomach
  • Moreover, if required, endotracheal intubation can still be performed by using a bougie through the SGA. This provides another option to perform ETI without interruptions of chest compressions.
  • And last but not least, SGA's allow continuous measurement of end-tidal CO2 ​
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Summary of Evidence and Experience on Airway-Devices used for CRP

The International Liaison Committee on Resuscitation (ILCOR) has again carried together all evidence and recently published more than 50 new ILCOR treatment recommendations and scoping reviews. You can find these documents right here: https://costr.ilcor.org 

This website provides an excellent systematic review of the Advanced Airway Management during Adult Cardiac Arrest, containing references to all relevant evidence available.


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​Based on this and given the experience from everyday clinical practice, it would be worth considering supplementing the recommendations as follows.

- For resuscitation performed by health care professionals (physicians, nurses, paramedics), the use of a supraglottic airway (ideally non-inflatable) as soon as possible is recommended.



2019 AHA Focused Updated on Adult Cardiovascular Life Support

​

Vitamin C in Sepsis - Fails!

20/1/2020

 
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​The headlines in the news 2017 were remarkable indeed: "Doctor believes he has found the cure for sepsis..." or "Doctor says improvised 'cure' for sepsis has had remarkable results".

Dr. Paul Marik described his observation in an interview in 2017, where he mentions several cases of sepsis that have almost miraculously responded to the application of vitamin c (watch here: Interview on WAVY TV). He even continues, that since then they see "the same thing over and over again". This implicated that these results were reproducible. He finally stated that the current data at that stage were "impressive" and that there was enough basic science to show that it works.

Vitamin C has many interesting properties that theoretically could be on benefit in sepsis. (read here: Crit☁ post on Vitamin C). Its application was already proposed for the treatment of other diseases like the common cold of Influenza. Despite some moderate positive influence observed, these results could not be reproduced in trials.

While the news picked up on this story as a miracle drug, Paul Marik et al. published their results of a before-and-after single-centre, retrospective cohort study in Chest 2017. In this paper, they compared 47 patients with sepsis that received the metabolic cocktail (Vitamin C 1.5g 6-hourly, hydrocortisone 50mg 6-hourly and thiamine 200mg 12-hourly) to 47 patients which did not - notably in a non-double-blinded, non-randomized fashion. Their results showed overall hospital mortality of 8.5% with the 'cocktail' and 40.4% without its application.​

This publication was reason enough to launch a small war of faith about sense and nonsense of this cocktail for sepsis.

​

The VITAMINS Trial - First Failure 

Since 2017 a tiny bunch of studies were published, many of them with significant limitations like a small number of patients, often not randomized-controlled and with conflicting results.

Nabil Habib T, Ahmed I (2017) Early Adjuvant Intravenous Vitamin C Treatment in Septic Shock may Resolve the Vasopressor Dependence. Int J Microbiol Adv Immunol. 05(1), 77-81.

Shin et al. J Clin Med. 2019 Jan; 8(1): 102.

Fowler et al. JAMA. 2019 Oct 1;322(13):1261-1270.


Fujii et al. have just now published the first more substantial and rigorous trial taking a closer look at the influence on vitamin c in sepsis.


They performed an

international, multicenter, randomized-controlled open label trial

In which they enrolled 211 patients with septic shock admitted to an ICU.

They compared

Treatment with Vitamin C 1.5g 6-hourly IV, hydrocortisone 50mg 6-hourly IV and thiamin 200mg 12-hourly IV

to

Hydrocortisone 50mg 6-hourly IV only.

They found

No difference in time alive and time free of vasopressors (primary endpoint) and

No difference 28 days or 90 days mortality (secondary endpoint)
This first study on a larger scale, unfortunately, disappoints. More trials are on the way and might give a clearer picture of this topic to come to a final decision eventually. 

For the moment it is appropriate to state:
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  • At this stage there is NO evidence to support the routine use of Vitamin C in sepsis
 
  • Sepsis is a complex syndrome and not a disease, it is unlikely a single substance will bring simple 'cure' to all patients
 
  • Why on earth does it seem that the use of steroids are basic mainstay of sepsis treatment?

​Just as a reminder: Guidelines recommend against the routine use of glucocorticoids in patients with sepsis. However, corticosteroid therapy is appropriate in patients with septic shock that is refractory to adequate fluid resuscitation and vasopressor administration.


Fujii et al. JAMA. Published online January 17, 2020. doi:10.1001/jama.2019.22176​

7 Reasons for the Use Vasopressors through Peripheral Catheters

16/12/2019

 
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​Teaching in medical school and opinions in literature are in agreement: The application of vasopressors requires central venous access. The reason for this are concerns that vasopressors given over a peripheral venous catheter (PCV) may cause phlebitis or even worse necrosis or ischemia through extravasation. 

​While irritation of a peripheral vein is often observed with the administration of drugs like potassium or amiodarone, this usually is not the case with the application of, e.g. norepinephrine. Besides, it is essential to keep in mind that the insertion of a central venous catheter (CVC) is technically demanding and takes a certain amount of time when performed correctly. The procedure is also associated with potentially dangerous complications that might be hazardous to the patient.

Therefore a fundamental question arises:

Do all patients that require vasopressors need a central venous catheter?
​

​

What about the peripheral access (PVC) - Any dangers there?


​Study #1

In 2015 Cardenas-Garcia et al. have published a 

​open-label, single-centre trial 

in which they treated

a total of 734 patients with the vasopressors noradrenaline (506), dobutamine (101 and phenylephrine 176 via peripheral access only.

The average duration of infusion was 49 hours.

They found


extravasation in only 2% of all patients without any further tissue injury following treatment with local phentolamine injection and nitroglycerin paste.
These findings indicate that:
​
  • Correctly applied vasopressors via a peripheral line are safe, even if given over several hours
  • Complications like extravasation are generally rare and are unlikely to cause any further harm​

J Hosp Med. 2015 Sep;10(9):581-5. doi: 10.1002/jhm.2394. Epub 2015 May 26.


​Study #2

In 2015 Loubani et al. performed a systematic review of extravasation and local tissue injury from the administration of vasopressors through peripheral intravenous catheters and central venous catheters. They looked at
​
  • Local tissue injury close to the infusion site
  • Extravasation of a vasopressor into surrounding tissue or a body cavity
  • Major disability of the patient

An excellent summary of this study can be found on REBELEM, who correctly states that this review was only for complications from administration of vasopressor, and not a review of the frequency of complications (i.e. instances where no complications occurred).

This review shows nicely though that
​
  • Most complications concerned peripheral IV-lines distal to the antecubital or popliteal fossae, and
  • Almost all occurred in infusions running for more than 4 hours

J Crit Care. 2015 Jun;30(3):653.e9-17. doi: 10.1016/j.jcrc.2015.01.014. Epub 2015 Jan 22


​Study #3

In 2017 Lewis at al. performed a retrospective chart review of 202 patients who received vasopressors through a PVL. The primary vasopressors used were norepinephrine and phenylephrine. The most common PVL sites used were the forearm and antecubital fossa. The incidence of extravasation was 4%. All of the events were managed conservatively; none required an antidote or surgical management. Although with many limitations to this review, there is further evidence indicating:

  • Extravasation seems to be a rather rare complication and again did not result in any further harm for the patient

J Intensive Care Med. 2017 Jan 1:885066616686035.


​Study #4

In 2018 Medlej et al. tried to determine the incidence of complications of running vasopressors through PIVs in patients with circulatory shock in a prospective, observational trial. Again, REBELEM has nicely summarized this rather small trial. It is another small indicator that:
​
  • In patients with shock, the use of peripheral vasopressors (noradrenaline and dopamine) in a large bore PVC at a proximal site for less than 4 hours is safe!

​J Emerg Med. 2018 Jan;54(1):47-53.


​Well, how do PVC's compare to CVC's then?


​Study #5

In 2018 Ricard JD et al. performed a

Multicenter, controlled, parallel-group, open-label randomized trial

in which

Patients were randomized to receive central venous catheters (135 patients) or peripheral venous catheters (128 patients) as initial venous access.

The primary endpoint was the rate of major catheter-related complications within 28 days.

They found significantly more PVC-related complications per patient when only treated with peripheral lines compared to patients that received at least one CVC.


And they concluded: "central venous catheters should preferably be inserted: a strategy associated with less major complications"
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REALLY? Hold on! - let's have a close look at those 'major complications, the PRIMARY endpoint of this study!

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Although going through this article several times, it remains difficult to understand how PVC insertion difficulties are comparable major complications.
First of all, difficult venous access is one of the indications for the insertion of a CVC, not its complication. Patients were randomly allocated in a one-to-one ratio to receive a CVC or a PVC. So how can difficult peripheral access be a complication when going for central access directly?
​
Also, there is considerable doubt whether the occurrence of a pneumothorax can be used to compare complications of these two procedures!


However, when eliminating difficult peripheral access as an indication, there is not much left to say PVCs are associated with more complications than CVCs. Moreover, most clinicians will agree that catheter infections in PVCs are less problematic than when occurring in CVCs.

Given these considerations, it seems safe to say:


  • In critically ill patients peripheral access can be tricky indeed
  • PVCs might be associated with more frequent local erythema and extravasation of fluids
  • Good to know: peripheral access is not associated with more pneumothoraces ; )

Crit Care Med. 2013 Sep;41(9):2108-15 


​2019 - More Evidence Keeps Rolling In!
​

Study #6

Tian et al. have performed a 

Systematic review 

in order to assess

 the frequency of complications associated with the delivery of vasopressors via PVCs.

They included

Studies of continuous infusions of vasopressor medications (noradrenaline, adrenaline, metaraminol, phenylephrine, dopamine and vasopressin) delivered via a PiVCs that included at least 20 patients. This resulted in seven observational studies (only) with a total of 1384 patients.

They found that

Extravasation occurred in 3.4% (95% CI 2.5-4.7%) of patients. There were no reported episodes of tissue necrosis or limb ischaemia. All extravasation events were successfully managed conservatively or with vasodilatory medications.


 
  • Extravasation seems to be an issue with PVCs, but there is no further information on the size or location of the peripheral line.
  • Again, no serious side effects were reported, indicating that peripherally administered vasopressors are safe over all when given for a limited duration.

Emerg Med Australas. 2019 Nov 7.


​Study #7

Pancaro et al. published

a retrospective cohort study

in which  identified


14'385 surgical patients who received peripheral norepinephrine infusions perioperatively with a concentration of 20 µg/mL (a rather low concentration)

They found

Extravasation of norepinephrine in only 5 patients and there where zero related complications requiring surgical or medical intervention. The median time of norepinephrine infusion among these patients was 20 minutes.
This is a fairly good indicator that:

  • Giving vasopressors through PVC for a limited duration is safe
  • Extravasation might actually be harmless when applied in rather lower contentrations

Anesthesia & Analgesia. SEPTEMBER 27, 2019

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Giving the current evidence available, it seems appropriate to conclude:

  • The need for vasopressors itself is not a mandatory indication for central venous access
 
  • Vasopressors can be safely given through a peripheral venous catheter
    • This is especially true when used for a limited time (e.g. less than 4 hours) and when applied in rather lower concentrations.
 
  • ​In the critically ill central venous access will inevitably still be required (advantage of multiple lumens, difficult peripheral access, other drugs that do entitle the use of a  CVC etc.)
​

A Flu Shot a Year keeps ICU Survivors Alive!

25/7/2019

 
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​Patients who have survived critical illness are at increased risk for long term morbidity and mortality. Maybe we tend to forget this fact, as we lose sight of these patients when they leave our unit. But this is especially true for ICU patients aged 65 and older!

There have been clues that influenza vaccination might reduce morbidity after surviving critical illness and Christiansen et al. have looked exactly into this topic.

The investigators examined whether an influenza vaccination (flu shot) affects the 1-year risk of myocardial infarction, stroke, heart failure, pneumonia, and death among ICU survivors aged 65 and older.

The investigators

Performed a nationwide population-based cohort study

They used the Danish Intensive Care Database

 To evaluate a total 89'818 ICU survivors from 2005 until 2015

It is noteworthy that 

Influenza vaccinated patients (these were 39% of all) were older, had more chronic diseases and used more prescription medications!

Their findings show that

1. Influenza vaccinated patients showed an 8% decreased risk of death and a 16% reduced risk of hospitalisation for stroke within one year

2. Cardiac surgery patients were the subgroup that profited most
​
3. Unfortunately, no significant association was found for the risk of hospitalisation for myocardial infarction, heart failure or pneumonia.

​

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The flu shot saves lives! This is another strong hint, that the influenza vaccination is clearly of benefit to all adults aged 65 and older. This is especially true for ICU survivors!


Christiansen at al. Intensive Care Med 
2019 Jul;45(7):957-967.


Also worth mentioning:
​
Not only influenza A but also Influenza B infection can pose a risk for severe secondary infection in previously healthy and younger persons. 


Aebi et al. BMC Infect Dis 
2010 Oct 27;10:308.

​

Dexmedetomidine - Sugar and Spice for the Mechanically Ventilated Patient?

10/7/2019

 
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When the FDA approved dexmedetomidine (DEX) in 1999, intensive care medicine had a novel and highly promising drug at its disposal. Compared to clonidine, dexmedetomidine is an 8 times more selective, central alpha 2 agonist, which binds to all 3 subtypes of the receptor. The properties of this substance were auspicious, among them: sedation, analgesia, neuroprotective effects and a lack of respiratory depression.

- Sedation decreases sympathetic activity, aggression and leads to a non-REM-like state, which of all sedatives comes closest to natural sleep. Cognitive functions are maintained, and patients usually remain arousable. 

- Dexmedetomidine has a particular analgesic effect via modulation in the region of the posterior horn of the spinal cord. This has shown to reduce the use of opiates.

- By reducing cerebral catecholamines, dexmedetomidine exerts a neuroprotective effect.

- Interestingly, sedation with dexmedetomidine is not associated with significant respiratory depression.

These properties pointed to a wide range of applications in the intensive care unit:

- Sedation in patients with non-invasive ventilation
- Weaning of invasively ventilated patients
- Agitated delirium
- Treatment of various withdrawal syndromes
- Fiberoptic awake intubation in theatre conditions

Dexmedetomidine comes with its side effects, though. Most commonly bradycardia and hypotension are observed, making second and third-degree heart block a contraindication. Also, nausea and a dry mouth might be seen.

Interestingly, prolonged use might be associated with some extent of discontinuation syndrome similar to clonidine. This involves hypertension, tachycardia, nervousness etc.
​


What Evidence Do We Have So Far?
​

Current data indicate that dexmedetomidine, compared to benzodiazepines: 

- Might reduce the duration of sedation in mechanically ventilated patients, JAMA. 2007 Dec 12;298(22):2644-53.

- Might improve performance in patients with sepsis in regards to delirium, coma-free days and maybe even survival, Crit Care. 2010;14(2):R38. PMC2887145.


- Seems to reduce delirium in ICU and the need for mechanical ventilation in critically ill patients, JAMA. 2009 Feb 4;301(5):489-99.

- Seems to allow earlier extubation in mechanically ventilated patients and makes them more alert to communicate pain, and

- Compared to propofol, dexmedetomidine was comparable in terms of duration of mechanical ventilation, length of stay in ICU and hospital and also the incidence of hypotension and bradycardia. JAMA. 2012 Mar 21;307(11):1151-60. 

- Some further evidence indicates that dexmedetomidine might be helpful in the treatment of mechanically ventilated patients with agitated delirium, resulting in more ventilator-free days. JAMA. 2016 Apr 12;315(14):1460-8.

According to all this, the question arises, whether we should use dexmedetomidine early in ventilated, critically ill patients.

The SPICE III Trial

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Precisely this question was now addressed by Shehabi et al., published in the NEJM

They performed an


International (8 countries, 74 ICU's), randomised controlled, unblinded trial

In which they evaluated

4000 ICU patients that were expected to need mechanical ventilation for at least 48 hours and required sedation for safety or comfort

They compared

Patients sedated with propofol, midazolam or other agents as prescribed by the treating physician with patients receiving dexmedetomidine as a continuous infusion 
(if DEX alone was insufficient, other agents could be added! In fact, 64% of patients also received propofol, 3% midazolam and 7% received both)


They found

1. No difference in 90-day mortality (primary outcome) and

2. No difference in death after 180 days, institutional dependency at 180 days, mean cognitive decline and assessment of the quality of life. Also no difference in median days free from coma to day 28 and median ventilator-free days at day 28 (all secondary outcomes)

3. Dexmedetomidine was though associated with significantly more events of bradycardia, hypotension​ (no further info on the use of vasopressors) and asystoles (14 vs 2; 7 required mechanical resuscitation measures)
​
​
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​- DEX is an attractive sedative in certain situations (alcohol withdrawal, other forms of delirium, weaning process etc.), BUT

- DEX doesn't seem to provide any advantage in the sedation of mechanically ventilated patients in the ICU and

- Might be problematic due to adverse cardiovascular effects, especially in this group of patients


Shehabe et al. 
N Engl J Med 2019; 380:2506-2517

Did you Know?

Apparently, intranasal dexmedetomidine seems used successfully for sedation in adults and children. J Clin Neurophysiol. 2019 May 16.

Crit.Cloud considered relevant for Critical Care Medicine Education by the Journal of Intensive Care Medicine

10/3/2019

 


​Top Ten Websites in Critical Care Medicine Education

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The Journal of Intensive Care Medicine has recently published a review of websites providing educational content that is part of the Free Open Access Meducation (FOAMed) movement. The authors have searched the web for critical care medicine education websites and have identified 97 sites they consider relevant for critical care.

These websites were then reviewed and evaluated using the Critical Care Medical Education Website Quality Evaluation Tool (CCMEWQET). They were then split up into three tertiles according to their score.

Congratulations to the Top Ten websites that indeed provide excellent educational information freely accessible.

Oh, and by the way we might mention that our small site Crit.Cloud has been considered among 96 other as relavant in this field and has ended up in the middle tertile with its ranking. 
🙃
​

A big thank you to the authors of this paper for their excellent work and for providing us with an updated list of websites worth taking a closer look! We are delighted to follow their wish by sharing the table of these websites.

​
Wolbrink TA et al. J Intensive Care Med. 2018 Jan;34(1):3-16

​

 Full List of all Website Reviewed (Click on a table enlarge)

Lasix for Acute Pulmonary Oedema?... An Overview

6/1/2018

 
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Just recently our ICU team was called to the wards to look at a 74-year-old gentleman with sudden shortness of breath and low peripheral saturation. He was known to suffer from hypertensive heart disease and now presented with acute pulmonary oedema. After giving oxygen over a non-rebreathing mask, he was administered furosemide (Lasix) intravenously and brought to the unit for non-invasive ventilation.

​Interestingly a discussion started on whether giving Lasix as a first line agent in the acute setting of pulmonary oedema is beneficial or not.  A quick look into to current literature gave no clear answer and reading further into the topic revealed unusual properties of Lasix we hadn't been really aware of so far. We all use and love Lasix, but do we really know the drug?​
​

The Beginning of Lasix

Furosemide (sometimes also called frusemide) was first developed by 'Farbwerke Hoechst AG' in Frankfurt am Main, Germany, a company that was founded back in the year 1863. Karl Stürm, Walter Siedel and Rüdi Weyer set the basis with the invention of N-substituted-3-Carboxy-6-Halo-Sulfanilamide, and it's derivates, one of them being furosemide. The researchers soon noticed its saluretic (sodium Na, potassium K and chloride Cl) and diuretic effect in almost equivalent proportions. As these substances did not cause any acidosis nor alkalosis, they suggested their future use for the treatment of oedema and hypertension.

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The Naming of Furosemide


Researchers soon noticed that the diuretic effect of furosemide lasted for about 6 hours... 'LAsts for SIX hours'... and therefore gave it the name: LASIX!

​

​

​
​What is Furosemide

​Furosemide is an organic anion from the group of loop diuretics (as are bumetanide and torasemide) and is sold under the brand name of Lasix©. Its indications are for the treatment of oedema due to heart or liver disease as well as kidney disease. It is also used for the treatment of mild or moderate hypertension. Furosemide has become one of the cornerstones in the treatment of heart failure.

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How does it work?

Furosemide can be applied by oral intake as a tablet or as an intravenous injection. Once in the bloodstream, it is predominantly bound to proteins (>90%).

Loop diuretics do not undergo glomerular filtration. In fact, they pass the glomerulus and are actively secreted across proximal tubular cells by organic anion transporters and the multidrug resistance-associated protein 4 (area A). It is important to know that non-steroidal anti-inflammatory drugs (NSAID) and endogenous uremic anions compete with this loop diuretic secretion and can cause 'diuretic resistance'.

Once loop diuretics have reached the tubular system, they bind to sodium-potassium-chloride co-transporters (NKCC2) in the ascending limb of the loop of Henle and block the reabsorption of these ions directly (area B). Further down at the macula densa they inhibit the same co-transporter (area B) thereby stimulating renin secretion and inhibiting tubuloglomerular feedback. This results in preserved glomerular filtration despite increased salt delivery to the macula densa. All this finally results in the loss of sodium, chloride and potassium and therefore loss of water.
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Other Effects

Furosemide also interacts with other sodium-potassium-chloride co-transporters (NKCC1) elsewhere in the body:
- Blocking NKCC1 in the ear probably explains the ototoxicity of loop diuretics
- Blocking NKCC1 in smooth muscle cells causes vasodilation
​- Blocking NKCC1 in the afferent arteriole and near the macula densa elevates renin secretion and the generation of angiotensin II

These complex interactions on haemodynamics explain that the net response in each patient might be different. On the one hand, loop diuretics dilate blood vessels directly and increase the level of vasodilatory prostaglandins. On the other hand, some of these effects counteract each other making it difficult to predict which effect will finally predominate.

Many studies have looked closer into the vasoactive properties of furosemide. Current evidence indicates that it has a systemic venodilator effect which actually reduced preload acutely. The same investigators found a reduction in the right atrial pressure and the pulmonary capillary wedge pressure, presumably reflecting the systemic venodilator effect of furosemide.​

While the acute venodilator effect may be beneficial to the failing heart, its action on arteries might be detrimental. Several studies have shown that in patients with chronic heart failure furosemide causes arterial vasoconstriction. Also, there is one study showing that pulmonary vascular resistance in healthy volunteers rose significantly. 

Francis GS et al. described how the administration of furosemide actually led to decreased LV function, increased LV filling pressures, increases in MAP, SVR, plasma renin activity, and plasma noradrenaline levels.​



Beneficial venodilator response predominates over arterial vasoconstriction in patients with (1) myocardial infarction and (2) salt depleted volunteers.

Venous relaxant effect has not been demonstrated in patients with chronic heart failure. In this setting detrimental arterial vasoconstriction seems to predominate.


Pardeep S et al. Br J Clin Pharmacol. 2000 Jul; 50(1): 9–13.

Francis GS et al. Ann Int Med 1985; 103(1): 1-6.



Pharmacological Properties

Administered furosemide orally has a limited and highly variable bioavailability. The diuretic effect starts within the first hour, and the duration of action is around 6 hours (4-8 hours). Injected furosemide intravenously is approximately twice as potent on a per-milligramme basis as oral doses. 

In acute decompensated heart failure sodium retention becomes more avid and higher peak levels might be required to become more effective. This can be achieved by giving furosemide intravenously.

Once a loop diuretic is administered, the excretion of sodium chloride is increased for several hours. This is then followed by a period of very low sodium excretion resulting in a so-called 'post-diuretic retention'.​



How to use Furosemide for Acute Decompensated Heart Failure (ADHF)

So far for the basics of furosemide, but what about its usage for acutely decompensated heart failure? Should furosemide be given as soon as possible or not?


The 2013 ACCF/AHA guidelines for the management of patients with heart failure give diuretics a class I recommendation. The evidence behind these recommendations though is level B or level C only! So these recommendations are not really helpful to answer this question.

The authors in UpToDate® mention diuretics directly after the use of oxygen. For patients with evidence of volume overload their recommendation is to give loop diuretics immediately (Grade 1B) as there is evidence that in this setting this may improve outcomes. They also suggest that patients with ADHF usually are volume overloaded, therefore indicating that most patients should receive diuretics ASAP.  
The only exception they mention where some delay in inducing diuresis might be required is in patients with severe hypotension or cardiogenic shock.

There is reasonable doubt that patients with ADHF are usually volume overloaded, as suggested by UpToDate®. Zile MR et al. demonstrated that while most patients with acute pulmonary oedema have increased filling pressures, most did not have significant increases from their dry weight on presentation! Fallick et al. actually argue that it isn't fluid gain but rather shift in fluids from other compartments, mainly shift from the splanchnic circulation, which usually is very compliant.

And as mentioned above, there is evidence that giving a straight shot of furosemide might actually influence haemodynamics negatively in different ways (decreased LV function, increased LV filling pressures, increases in MAP, SVR, plasma renin activity and plasma noradrenaline levels).

In conclusion there is no straight forward answer to this question, but I would put it down as follows:

​
​
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​
​- Furosemide should not be routinely used for the immediate treatment of acute decompensated heart failure (ADHF)/ acute pulmonary oedema

- However, in patients with evidence of volume overload the administration of early furosemide (preferentially given as an intravenous bolus) seems beneficial and  improves outcome. But beware, most patients are not volume overloaded!

- In urgent situations the focus should be on early non-invasive ventilation and the administration of nitroglycerin!


David H et al. N Engl J Med 2017;377:1964-75.

Wilson S et al., UpToDate.com 2018


WRITING COMMITTEE MEMBERS, Yancy CW, Jessup M, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation 2013; 128:e240.

Zile MR, Bennett TD, St John Sutton M, et al. Circulation 2008 Sep 30;118(14):1433-41

Fallick C et al. Circ Heart Fail 2011; 4: 669-75.

​

Intraoperative Ketamine: A Big Hooray for Special K?

3/6/2017

 
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Postoperative pain and delirium is a common concern and currently approached by different interventions. There is  some evidence suggesting that ketamine given intra-operatively might have an influence on postoperative pain and delirium. Some anaesthetists commonly give a single dose of ketamine intra-operatively for exactly this reason.

Thumbs up for Ket

Ketamine has kept its fascination in various settings, from retrieval medicine onto the the care of critically ill patients in the ICU.  Ketamine reduces postoperative markers of inflammation, is a rapid-acting antidepressant drug with an effect lasting for several days and might have neuroprotective properties. 

Ketamine also has become increasingly popular as an adjunct to other sedatives in the ICU. There is evidence showing that ketamine used in the ICU has the potential to reduce cumulative opioid consumption after surgery (Asad E. et al. J Intensive Care Med December 8 2015 ).


Even better: It does not cause any kidney injuries, preserves laryngeal protective reflexes, lower airway resistance and much more...

And: Ketamine is cheap and has been used safely for over 50 years by anaesthetists!

The Dark Side of Ket

But there's the other side of ketamine making all of this a little more complicated. After all, Ketamine is a psychoactive drug and has well known hallucinogenic properties. Developed in the 1960s as a dissociative anaesthetic agent it started to appear on the street in the early 1970s and made its way to the 1980s as Special K, Acid and Super C (Dotson JW et al. J of Drug Abuse, Vol 25, Issue 4, 1995).

From a medical point of view there are some worries that these psychotomimetic effects, which are of concern in the critically ill patient, might predispose to delirium (Erstad BL, J Crit Care, Oct 2016, Vol 35, p 145-149​).

The PODCAST Trial

On the background of all this facts this trial revealed some interesting findings. Avidan et al. performed a

multicentre, international randomised trial

in which they randomly assigned

672 patients undergoing major cardiac and non-cardiac surgery under general anaethesia

into three groups to either receive a bolus of

placebo (normal saline), low-dose ketamine (0·5 mg/kg), or high dose ketamine (1·0 mg/kg) after induction of anaesthesia, before surgical incision.

 Participants, clinicians, and investigators were blinded to group assignment. They found

NO difference in in the incidence of postoperative delirium among these groups

but

significantly more postoperative hallucinations and nightmares with increasing ketamine doses compared to placebo
This trial seems well performed with an acceptable sample size. The application of a single dose of ketamine before surgery neither prevented delirium nor induced it. With this sample size it seems safe to say that even if ketamine does prevent delirium, its effect would be rather small.

Furthermore, postoperative pain was not influenced by giving a single dose of ketamine and this is in contrast to previous findings and current guidelines. Importantly, most of the previous studies are smaller than this trial, making these findings remarkable.

But what really drew my attention was the fact that the appearance of hallucinations and night-mares was increased for at least 3 days after surgery.  

So if ketamine has no influence on postoperative delirium or pain but does induce hallucinations and nightmares, even 3 days after surgery, current guidelines might have to be revised.

The Bottom Line

- The application of a subanaesthetic dose of ketamine during surgery to tackle postoperative pain and delirium does not seem to be as effective as previously assumed

- The usage of ketamine in this setting even seems to have undesirable side-effects like hallucinations and nightmare - and this effect might even last for up to 3 days!

- This trial provides good reasons to look for other options to prevent postoperative delirium!


(Like dexmedetomidine? The answer to this question has just been answered: READ HERE!)

​Avidan MS et al. The Lancet, May 30th 2017


Vitamin C - To the Rescue?

26/3/2017

 
Sometimes there's this moment you read about medical research in the news... sometimes you read lots of rubbish on medical issues in the news... but sometimes you stop and read, and you don't know what to think. This happened to quite some of us a couple of days ago when reading the headlines in the British Independent:
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Well, it's not very often you read the term sepsis in the news but the word 'cure' causes estonishment or rather misbelief.  Further reading certainly catches your attention: 'A doctor in the US state of Virginia claims to have found his own cure for sepsis' and 'Since then, he has used it to treat 150 sepsis patients.  Just one has died of the condition, claims Dr Marik'. And it's not an article from some remote pseude magazine... no, it has been published in 'Chest'! And all this is not due to some novel molecule... it's all about Vitamin C!

Thanks to #FOAMed quite some smart brains have looked into this topic already... 

So here's the most important facts you need to know - in short:

What's the Story?

Paul Marik et al. have published  a 

single-centre retrospective cohort study 

in which they have treated

47 consecutive septic patients over a periode of 7 months with intravenous vitamin C (1.5g 6-hourly), hydrocortisone (50mg 6-hourly) and thiamine (200mg 12-hourly)

and then compared these patients to

47 septic patients treated in their unit during the preceding 7 months

They performed

Propensity score matching

and found 

An overall hospital mortality of 40.4% in the control group compared to 8.5% in the intervention group

This means

An absolute risk reduction of 31.9% and also according to the authors none of the patients in the intervention arm died of sepsis!

What Does This Mean?

These results are quite amazing on the first look, but there's more behind these numbers. Paul Marik has first of all published an observational study: unblinded, uncontrolled, retrospective and low in patient numbers.

There are several limitations that go hand in hand with studies as such and unblinded before-and-after studies have a lot. A major challenge in conducting observational studies is to draw inferences that are acceptably free from influences by overt biases, as well as to assess the influence of potential hidden biases. One of the biggest drawbacks in this current study is the timely/ seasonal difference when patients have been selected.
If you are interested to have a closer look on this you should read Dan's blog entry on stemlynsblog.org HERE. 

Studies like this one are an important part of science,
but observational studies are observational... not proof!
​

Why Vitamin C in Sepsis?

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There is a scientific rationale behind all of this. As mentioned by Paul in his paper vitamin C levels do fall low in sepsis and the most efficient way to administer it is intravenously. The same is true for thiamin which also goes low in up to one third of all septic patients.

There are two rather small randomised control trials suggesting that vitamin C is safe in septic patients and might actually be of some degree of benefit for the patient.

Vitamin C

- Neutralizes free radicals and has therefore antioxydative properties 

- Is an important conenzyme for the procollagen-proline dioxygenase, which itself is necessary for the biosynthesis of stable collagen in our body. Vitamin C deficiency leeds to unstable collagen and therefore scurvy

- Is an important cofactor in the synthesis of steroids like cortisol and catecholamines like dopamine and noradrenalin as well 

- and it has many more functions that go beyond the scope of this blog entry!

However, the importance of vitamin C in the treatment and prevention of diseases like e.g. the common cold or influenza remains highly contrversial. The observation of some moderate positive influence on the course of disease in some studies could not be reproduced in other trials. 

Under normal circumstances vitamin C deficiency is practically non-existent in Europe, but becomes a fact during sepsis. 
If this is clinically relevant in septic patients seems plausible but remains to be elucidated.

​
Shailja Chambial, Shailendra Dwivedi, Kamla Kant Shukla, Placheril J. John, and Praveen Sharma. Vitamin C in Disease Prevention and Cure: An Overview. Indian Journal of Clinical Biochemistry. Oktober 2013; 28(4): S. 314–328

H. Hemilä, E. Chalker: Vitamin C for preventing and treating the common cold. Cochrane Database of Systematic Reviews. 2013

R. M. Douglas, E. B. Chalker, B. Treacy: Vitamin C for preventing and treating the common cold. In: Cochrane Database of Systematic Reviews. 2000; 2:CD000980.

Another great read into the details: Josh Farkas from pulmcrit
​

More Ifs and Buts

Sepsis is not a disease, its a clinical syndrome that has physiologic, biologic and biochemical abnormalities caused by a dysregulated inflammatory response to infection. The fact that different definitions have evolved since the early 1990s shows that we still struggle to definde sepsis as a single entity. This is one reason why a single therapy might not always be the best for each diesease causing sepsis.
 
Paul Marik’s publication is interesting and deserves respect. It’s an observational study but provides no evidence by far. Vitamin C might be an interesting novel approach to sepsis but the term ‘cure’ used in the media is inappropriate and misleading.
 
The term ‘cure for sepsis’ also implicates that vitamin C is a cure for all infections causing sepsis and is therefore problematic.
​

The Current Bottom Line


​- The study published by Marik et al. is purely observational and provides no proof at all.

- Just because vitamine C might be safe in Sepsis does not mean this has to be given. At this stage no recommendation can be made for the use of vitamin C in sepsis.

- Studies like these are an part of research itself - However, the use of the term 'cure' seem problematic and inappropriate in this context.


Marik et. al, J Chest 2017

Close to the Proof: IV Contrast Media for CT-Scans Do Not Cause Acute Kidney Injury

27/1/2017

 
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When filling out the form for a CT scan in you hospital you will not only have to provide clinical information about the patient but almost certainly also the latest creatinine levels. This information is required as many clinicians are worried that IV contrast media might cause iatrogenic acute kidney injury and therefore increased rates of dialysis, renal failure, and death. Despite several reports of contrast-induced nephropathies in the past, the causal relationship between IV contrast media and the development of acute kidney injury has been challenged recently (Read our previous summary​ HERE).

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The major problem is that performing a randomized controlled trial to elucidate the true incidence of contrast-induced nephropathy is considered unethical because of the presumption that contrast media administration is a direct cause of acute kidney injury.

While the discussion goes on Hinson et al. have come up with another nice piece of evidence that in emergency situations there is no reason to withhold the application of IV contrast for CT scans when required.

​In this single-center retrospective cohort study researchers have included a total of 17'934 patient visits to their emergency department over a period of 5 years. They analysed three patient groups that where demographically similar: contrast-enhanced CT, unenhanced CT and no CT scan performed. Patients were included when their initial serum creatinine level was between 35 umol/L and 352 umol/L. Of all CT scans, 57.2 percent were contrast-enhanced. The probability of developing acute kidney injury was 6.8 percent for patients undergoing contrast-enhanced CT, 8.9 percent for patients receiving unenhanced CT and 8.1 percent for patients not receiving CT at all. This proofs to be the largest controlled study of its kind in the emergency department and shows that:

In current clinical context, contrast media administration for CT scans is NOT associated with an increased incidence of acute kidney injury. And even though a large randomised controlled trial is still missing it seems safe...

​
To Conclude:
​
There is no reason to withhold the use of IV contrast media in cases where contrast-enhanced CT is indicated to avoid delayed or missed diagnosis of critical disease.



Hinson J et al. Annals of Emergency Medicine, 2017; DOI: 10.1016/j.annemergmed.2016.11.021     OPEN ACCESS

Crit Cloud Review from 18/01/2015

Out-of-Hospital Cardiac Arrest: The Power of Adrenaline and Amiodarone

29/7/2016

 
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For the resuscitation out-of-hospital one of the mainstays besides compression and defibrillation ist the application of adrenalin and amiodarone. According to the new ACLS guidelines 2015 these are the only drugs remaining in the treatment for shockable rhythms.

​While adrenaline is given for maximum vasoconstriction in order to promote coronary perfusion pressure CPP, amiodarone and sometimes lidocaine are used to promote successful defibrillation of shock-refractory ventricular fibrillation VF or pulseless ventricular tachycardia VT. While the usage of these drugs is undoubtedly very effective in patients with existing circulation the effectiveness during resuscitation remains a matter of debate.

The Effect of Adrenaline

As a matter of fact it has never been proven that adrenalin actually improves long-term outcome. In 2014 Steve Lin and colleagues published a systemativ review on the efficacy of adrenaline in adult out-of-hospital cardiac arrest (OHCA). They were able to show that according to current evidence standard dose adrenaline (1mg) improved rates of survival to hospital admission and return of spontaneous circulation (ROSC) but had no benefit in means of survival to discharge or neurologic outcomes.

What about Amiodarone and Lidocaine?


Kudenchuck et al. now made the effort to look into the efficacy of amiodarone and lidocaine in the setting of OHCA. Used according to the ACLS guidelines 2016 amidarone is given after the third shock applied when treating a shockable rhythm. Two rather small controlled trials have shown so far that using amidarone actually does increase the likelihood of ROSC and the chance to arrive at a hospital alive. It's impact on survival to hospital discharge and neurologic outcome though remains uncertain.

In this randomized, double-blind trial, the investigators compared parenteral amiodarone, lidocaine and saline placebo in adult, non-traumatic, OHCA. They ended up with 3026 patients meeting inclusion criteria and which were randomly assigned to receive amiodarone, lidocaine or saline placebo for treatment. They finally found that neither amiodarone nor lidocaine improved rate of survival to discharge or neurologic outcome significantly. There were also no differences in these outcomes between amiodarone and lidocaine. Across these trial groups also in-hospital care like frequency of coronary catheterisation, therapeutic hypothermia and withdrawal of life-sustaining  treatments did not really differ, making a bias due to treatments after admission unlikely.

Take Home

- This study was not able to show any benefit of amiodarone or lidocaine in the the setting of OHCA  in terms of survival to hospital discharge and neurologic outcome

- Amiodarone seems to improve the likelihood of ROSC and survival to hospital admission (similar to adrenaline)

- As there are no other options, I believe amiodarone should remain part of the standard treatment for shockable rhythms in OHCA

- Lidocaine can be safely removed from CPR sets as there is no benefit of over amiodarone

​
Read here:

N Engl J Med 2016;374:1711-22

Resuscitation, June 2014, Vol 85, Issue 6, p 732-740


New ACLS Guidelines 2015, The Changes

From Review to Practical Guidance on How to Use Ketamine in the ICU

24/6/2016

 
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As posted on BIJC before, Asad et al. had performed a systematic review on the usage of ketamine as a continuous infusion (>24h) in intensive care patients. The same authors have now published a narrative review providing a more depth discussion about the pharmacological and pharmacokinetic properties of ketamine. Also they present recommendations for dosing and monitoring in an ICU setting.

The Goodies of Ket

Current evidence shows that Ketamine... 

- Has no adverse effects on the gastrointestinal tract (bleeding) and does not cause acute kidney injury (compared to nonsteroidal anti-inflammatory drungs, NSAID's) 

- Does not negatively influence bowel motility (in contrast to opioids)

- Preserves laryngeal protective reflexes

- Lowers airway resistance

- Increases lung compliance

- Is less likely to cause respiratory depression

- Is sympathomimetic, facilitates adrenergic transmission and inhibits synaptic catecholamine reuptake, therefore increasing heart rate and blood pressure

The Concerns of Ket

Ketamine...

- Might increase pulmonary airway pressure and therefore aggravate pulmonary hypertension

​- Might cause well known psychotomimetic effects which are of concern in the critically ill patient as this might predispose to delirium

- Interacts with benzodiazepines via the P450 pathway which could result in drug accumulation and prolonged recovery
​

Concerns Proven Wrong

- Ketamine need not to be avoided in patients at risk for seizures, particularly when used for analgosedation for short periods in the ICU setting

- Current evidence shows no increased intracranial pressure or associated adverse neurologic outcomes associated with ketamine administration in critically ill patients
​

Take Home 

The use of ketamine for analgosedation in the ICU continues to lack high-level evidence.However, it is effectively used around the globe and remains an attractive alternative agent for appropriately selected patients. Taking current knowledge and evidence into account this is especially true for patients with severe pain unresponsive to conventional therapies.

Taking precautions and contraindications into account ketamine is considerably safe and even avoids potentially adverse side effects of other agents used.


Erstad BL, J Crit Care, Oct 2016, Vol 35, p 145-149
​
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