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  • Summaries & Reviews
    • Airway
    • Cardiovascular
    • Controversies
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    • Infections
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    • Pharmacology
    • Procedures
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Reviews and Summaries

Acute myocardial infarction - It's pain radiating to the right arm we have to worry about!

15/3/2019

 
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​It was only back in in 1987 when William Heberdeen (not to confound with William Heberdeen, a London doctor who described the Heberdeen nodes back in the 18th century) published the first description of ischemic chest pain. It was the birth of the classical image of strangling chest pain that occasionally radiates to the left arm, associated with exertion and relieved by rest.

A recent publication in the BMJ shows, that positive troponin levels are found frequently in patients with non-cardiac problems. This finding underlines the importance of good history taking, including the assessment of chest pain (CP) characteristics. 

​

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Circulation. 2018;138:e618–e651. (Click image for link to article)


​
The TRAPID-AMI Study
​

McCord J et al. have taken a closer look at chest pain and associated symptoms and their association with the diagnosis of acute myocardial infarction. They also analysed these symptoms in relation to the size of the AMI.

They performed an


international, multicenter diagnostic study

in which they evaluated 

1282 patients admitted for possible AMI to emergency departments in Europe, the US and Australia

The outcome was

the correlation of symptoms with the diagnosis of AMI and its relation to myocardial infarction size

They found that

1. only 4 symptoms were independently predictive of AMI

- Radiation to the right arm/ shoulder (OR 3.0, CI 1.8-5.0)
- Chest pressure (OR 2.5, CI 1.3-4.6)
- CP worsened by physical activity (OR 1.7, CI 1.2-2.5)
- Radiation to left arm/ shoulder (OR 1.7, CI 1.1-2.4)


2. Patients with more than 1 of the 4 symptoms were more likely to have AMI
- For patients who had all 4 symptoms, 55% had a diagnosis of AMI


3. Patients with larger AMI's were more likely to have 
- pulling CP
- pain in the right upper chest (right supramammillary area)
- and right arm/shoulder radiation


​
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​- It's time to get rid of the classical image of CP radiating only into the left arm. While this might still be the predominant complaint at presentation, it's the right sided shoulder/ arm pain we should keep a close eye on!

- Chest pain radiating to the right shoulder/ arm is more predicitive of myocardial infarction than left sided chest pain

- And remember: a positive Troponin alone does not fullfill the diagnostic criteria of AMI!



Crit Pathw Cardiol. 2019 Mar;18(1):10-15.
​

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)

Handle an Iatrogenic Pneumothorax - Properly!

16/2/2019

 
Central venous lines a commonly used in critical care and normally don't cause too many problems. They are though associated with potentially severe complications like infection, thrombosis, occlusion, bleed and of course pneumothorax on insertion. Although the usage of ultrasound guidance minimises the risk of the latter, there remains a restriction risk of this happening, giving you the challenge to solve this problem professionally. 

​

The Case

​A 67-year old lady needed the insertion of a central venous catheter during surgery, which the anaesthetist performed with the aid of ultrasound but of course under aggravated conditions. When brought into the critical care unit postoperatively she presented with no audible breathing sound on the right side of her chest. ​An ultrasound (US) of the right lung showed no visible pleural gliding, and in M-mode only 'sea' but no 'beach' or 'sand'.
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Left lung: Beach, Sea and Sky: No pneumothorax!
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Right lung: No Beach (no sand): Suggests pneumothorax!
​
​To estimate the extent of the pneumothorax, we performed a pa chest x-ray (CR), which confirmed the diagnosis. The image showed an apical interpleural distance of 3cm and laterally of 2-3cm. 
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​How often does this happen? Could I have prevented this complication? What would you do in this situation? To answer these and some other questions we performed a quick review of current literature and provide a short review.

​

Are iatrogenic pneumothoraces common?

​It's a fact: Iatrogenic injuries are an inevitable part of medicine. Emergent procedures performed in the emergency department (ED) present a higher risk for iatrogenic injury than in more controlled settings (Swain et al., 2005; Mort, 2004). This fact implies that you should NEVER perform a procedure if you cannot handle the potential complications. A procedural error followed by mismanagement increases the likelihood of morbidity and mortality immensely.

The incidence in the literature varies from 0 to 6%​ (numbers are higher in emergencies), bearing in mind, that depending on the control method used (US, CR or none), some are just not diagnosed. Subclavian vein insertion has been reported to have a higher incidence of pneumothorax than internal jugular vein insertion.

​

What can I do to prevent iatrogenic pneumothoraces?

- Make sure that there is an indication for central venous access (e.g. vasopressors in low to moderate doses are no absolute indication, PulmCC: Are central lines really needed for vasopressor infusions?)

- Use a standardized method of CVC insertion in your unit or institution

- Insertion by experienced physician (performing more than 50 CVC insertion a year) or at least his assistance has proved to lower the risk of pneumothorax
​
- The use of ultrasound during CVC catheterization reduces the time required for insertion and the rate of mechanical complications

​
​

How do I diagnose a pneumothorax

Iatrogenic pneumothorax might not cause any clinical symptoms, especially in the young and otherwise healthy patient. Symptoms might include chest pain (sometimes radiating to the ipsilateral shoulder), shortness of breath (to life-threatening respiratory distress) and less commonly cough, anxiety or malaise.

On examination, you might find tachypnoea, asymmetrical lung expansion, unilaterally decreased breath sounds. Cardiovascular findings might include tachycardia, hypotension, pulsus paradoxus and jugular venous distension (often present in tension pneumothorax). Subcutaneous emphysema and tracheal deviation might occur occasionally.

A definite diagnosis is made by performing chest radiography (CR), CT-scan or bedside ultrasonography (US). Supine chest radiographs are unreliable in making the diagnosis of pneumothorax, with a sensitivity value of 36%. US is more sensitive than supine CR and as sensitive as CT in the detection of pneumothoraces. Performance of US for the detection of pneumothorax is excellent and is superior to supine CR. Considering the ease of access and the outstanding clinical performance of US (numerous studies have described near 100% sensitivity and 90% to 95% specificity if a thorough examination is performed), current studies support the routine use of US for the detection of pneumothorax.​


- Clinical signs are unspecific and might not be present

- Ultrasonography is the first choice ​for the detection of pneumothorax

- For a general evaluation of the size of a pneumothorax, an erect chest x-ray in inspiration is recommended

- CT scans are only recommended for uncertain or complex cases
​


Does every central line need a chest x-ray after insertion?

CR of supine patients is not sensitive enough to identify hidden pneumothorax because the air initially dissipates within the nondependent and medial parts of the chest and therefore can be invisible on supine radiographs. Even upright CR can be challenging and unreliable. Also, CR is often performed immediately after CVC insertion and it is therefore possible that there is not enough time for the development of a pneumothorax large enough to be identified.

​- Routine CR after central line insertion is unreliable and not necessary: It's an inefficient screening tool!

- Current evidence supports the use of US to exclude iatrogenic pneumothorax


​

How do I treat an iatrogenic pneumothorax?

If a pneumothorax occurs during the insertion of a central line urgent action might not be necessary. If asymptomatic, you might proceed with the central line insertion when the patient is in urgent need. 

- If signs of a tension pneumothorax arise, a simple needle decompression or urgent chest drain is life-saving and allows for a continued controlled attempt of the central line on the same side (you can’t cause a pneumothorax twice).

- Never attempt a central line insertion on the opposite side to avoid bilateral iatrogenic complications!

- In the setting of iatrogenic pneumothorax the BTS guidelines on the management of spontaneous pneumothorax can be applied:
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​- Remember: If the inter-pleural space on CR is less than 2cm (some allow 3cm as an upper limit) and the patient remains asymptomatic, conservative treatment is appropriate!

- Apply nasal oxygen 3-5L/min (see below)

- A follow up chest x-rax after 12-24 hours is advisable.



Did you know?

When no supplemental oxygen is applied air is reabsorbed spontaneously by 1.25% of pneumothorax size per day. Oxygen administration at 3 L/min nasal canula or higher flow treats possible hypoxemia and is associated with a fourfold increase in the rate of pleural air absorption compared with room air alone.

​

Got interested? Get more info here:
​


​
Pneumothorax as a complication of central venous catheter insertion, N. Tsotsolis et al. Ann Transl Med. 2015 Mar; 3(3): 40. OPEN ACCESS

Management of spontaneous pneumothorax: British Thoracic Society pleural disease guideline 2010, A. MacDuff et al. Thorax. 2010 Aug.​ OPEN ACCESS

Ding W. et al. Diagnosis of pneumothorax by radiography and ultrasonography: a meta-analysis. Chest. 2011 Oct;140(4):859-866.

Contou D et al. Small-bore catheter versus chest tube drainage for pneumothorax. Am J Emerg Med. 2012 Oct. 30 (8):1407-13. 

Rami A. et al. Iatrogenic emergency medicine procedure complications and associated trouble-shooting strategies: A narrative review: https://doi.org/10.1108/IJHCQA-08-2017-0157 OPEN ACCESS

The Postoperative 'Silent' Central Anticholinergic Syndrome

26/1/2019

 
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Just recently a 75-year-old gentleman was admitted to our unit as he remained unresponsive after short procedural sedation with Propofol. Although he was hemodynamically stable and showed proper spontaneous breathing at any time, the intervention team was concerned about his condition.

On arrival to our ICU, the patient was noted to be still unresponsive. He showed no reaction to painful stimulation. The Pupils were rather wide, but symmetrical in size and showed a prompt response to light. Brain stem reflexes were present and peripheral reflexes were triggerable. His breathing pattern was regular, and saturation levels were above 96% on room air. A blood gas analysis showed a normal pH and normal CO2-levels.

As usual, the common reflexes started to kick in, and some suggested to go for a CT-scan of his head to out-rule some significant complications. Luckily enough, close observation revealed some slow improvement of his alertness, and we considered the possible diagnosis of a central anticholinergic syndrome (CAS).

After the application of 1mg of physostigmine (2x0.5mg) intravenously the patient almost promptly awoke and had an uneventful stay on our unit.

This case just reminded me of these many patients in anaesthesia that inexplicably show delayed awakening after sedation or a general anaesthetic.

​
In fact, it is estimated that the incidence of  central anticholinergic syndrome is around 8- 12 % following general anaesthetic and lesser with regional anaesthesia.
​

What is a Central Anticholinergic Syndrome?

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​Classically the central anticholinergic syndrome (CAS) describes a condition where a substance causes a competitive antagonism of acetylcholine (ACh) at peripheral and central muscarinic receptors. Initially, these were plants containing atropine, hyoscyamine and scopolamine.

There are four muscarinic receptors:


- M1 ​​mainly in the central nervous system (responsible for delirium when antagonised)
- M2 in the brain and heart
- M3 in the salivary glands and
- M4 in the brain and lungs

The PERIPHERAL SYNDROME presents with:

- Dry mouth
- Difficulty swallowing (lack of saliva)
- Photophobia and blurred vision (due to dilated pupils)
- Dry skin, fever
- Reduced bowel sounds and urinary retention

The CENTRAL SYNDROME presents with:

- Agitation, agitated delirium, visual and auditory hallucinations
- Hypoactive delirium may also occur, this seems to be more common though in the postoperative setting

The clinical diagnosis of a CAS is more straightforward when typical peripheral symptoms accompany central signs.
​

The Problem with the "Silent" Postoperative CAS


​The clinical diagnosis of a CAS is often straight forward when typical central symptoms accompany peripheral symptoms. The problems are patients in the postoperative setting, ​in which the patient often presents with somewhat atypical central symptoms and often minimal or even no peripheral symptoms at all.

​Especially in this setting, the anticholinergic syndrome may be accompanied by sedation or coma. The mechanisms causative for this phenomenon are not well understood but might include greater tolerance at peripheral receptors, longer persistence at central receptors or greater CNS susceptibility due to age or disease.

Postoperative CAS is often associated with atypical central symptoms and minimal or even no peripheral signs at all! Sedation and coma are often observed in this setting.
​
​

What Drugs Cause CAS?


​Common anticholinergics agents should be more accurately referred to as antimuscarinics, as these agents do not generally block nicotinic receptors.
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A. H. Dawson, Br J Clin Pharmacol, Nov 2015

The Problem is that many currently used drugs in anaesthesia and critical care are also known to cause this syndrome.

This includes:


Benzodiazepines, opioids, phenothiazines, butyrophenones, ketamine, etomidate, propofol, nitrous oxide, and volatile inhaled anaesthetics!
​


How Can I Diagnose a "Silent" Postoperative CAS?


​The fact that postoperative CAS often lacks the presence of peripheral symptoms makes the diagnosis challenging. The different presentation of the syndrome ranging from somnolence, confusion, amnesia, delayed recovery, stupor, coma to agitation, hallucinations, dysarthria, ataxia, delirium makes it difficult to diagnose accurately.

It is, therefore, a diagnosis of exclusion! The most helpful tool you have is physostigmine!
​
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​The prompt arousal of a patient after the application of intravenous physostigmine is highly suggestive of a postoperative central anticholinergic syndrome.​
​
​

How to Use Physostigmine


​When dealing with prolonged somnolence or unexplained agitation following any form of anaesthesia, make sure to check and monitor vital signs and provide basic or advanced life support if necessary. 

Exclude common causes first (e.g. overhang of sedatives or opioids, persistent muscular paralysis, hypoxemia, hypercapnia, hypoglycemia and other). 

If common causes can be excluded and CAS is a probable diagnosis, you should consider the application of intravenous physostigmine.

Physostigmine in recommended doses is considered safe! Possible adverse effects are considered unlikely. Studies found cholinergic symptoms sometimes to be mild, and these adverse effects are more an indication of probable excessive doses rather than an established safety concern.

For postoperative CAS a dose of 1mg of physostigmine i/v is recommended.

This dose can be divided into two doses of 0.5mg i/v if required.

The maximum dose recommended in this setting is 2mg i/v.


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​Beware: You are giving Physostigmine Salicylat - Do not give to patients with aspirin allergy!

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​Read more here:

Cohen S, J Clin Anesth. 2006 Aug;18(5):399-400

Brown DV, Am J Ther. 2004 Mar-Apr;11(2):144-53

Br J Clin Pharmacol. 2016 Mar; 81(3): 516–524

BJA: British Journal of Anaesthesia, Volume 101, Issue eLetters Supplement, 29 December 2008

Take a very, very, very Close Look at this Nature Publication - or- What a Presidential Portrait Has to Do with a Heap of Feces

17/12/2018

 
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Updated 28/01/2019

While this website concentrates on finding relevant publications from the world of Critical Care, there are always papers from other fields that attract our attention.
Recently, a remarkable detail from a publication of an even more noteworthy journal has been brought to our notice. I admit I rarely read articles on 'Nature', but this article is worth a very close look after all.

Chiou L. et al. have published an article about a noninvasive genomic sequencing of populations from faeces in this years January issue of Scientific Reports of 'Nature'. In this article, they deal with the problem that it is difficult to obtain high-quality samples for genomic studies from wild animals. They, therefore, describe a cost-effective method for enriching host DNA from noninvasive faecal samples.

And in fact, it is worthwhile to have a closer look at the faeces sample in this article as Nature has placed a portrait of Mr Trump in a rather delicate position.​


Finding the hidden Trump-Portrait, here's how:

Update 28/01/2019:  The authors have reacted and changed the resolution of the image so that a closer zoom is no longer possible. Following instructions refers to the previous publication.​ 

1. Open the article in pubmed (just to proof, it's no fake news): 

Chiou KL et al. Scientific Reports, 2018 January 31: Methylation-based enrichement facilitates low-cost, noninvasive genomic scale sequencing of populations from feces​ 


2. It's OPEN ACCESS! Open the article via the full text links on the top right.
​


3. Download the pdf version of the article.


4. Go to page 3, figure 1. Spot the heap of feces right behind the pavian?
​


5. Zoom in on that heap of feces... zoom in closer... even closer!


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This publication impressively demonstrates the interdependence of science and politics.

Remember, sometimes the unexpected lies in the detail.

Did the editors of Nature actually realise this?

Update 28/01/2019: Well, obviously they now have!



OPEN ACCESS: Chiou KL et al. Scientific Reports 2018 January 31: Methylation-based enrichement facilitates low-cost, noninvasive genomic scale sequencing of populations from feces

Manage Critical Bleedings in Anticoagulated Patients like a Pro!

5/12/2018

 
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Anticoagulated patients are common, and the amount of available oral anticoagulants is becoming more diverse and confusing. Anticoagulation is the cornerstone in the treatment of thrombosis and thromboembolic complications in a variety of diseases. Lixiana, Pradaxa, Eliquis and Xarelto are some of these pretty-sounding drugs that many doctors know but find it difficult to keep up.

So if you work in an emergency room, anaesthesia or intensive care, there's a good chance you will be facing an anticoagulant patient with potentially critical bleeding that could require urgent treatment... And this leaves you with the following questions:​

- What is a critical bleed (apart from obvious massive bleeding)? Does this bleeding need imminent reversal?

- Do I need any laboratory testing before?

- What treatment should I actually give the patient?


If you do not have a guideline in your institution, it may be time to create one, and the following publication is indeed very useful for this purpose!​

The 2017 ACC Expert Consensus Decision Pathway on Management of Bleeding in Patients on Oral Anticoagulants very nicely summarises current evidence and expert opinion on these issues. But the very best are their excellent figures, providing all the answers you need: simple and very understandable!

What is a Critical Bleeding?

Picture


​Do I Need any Laboratory Tests Before?

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​What Treatment Should I Give the Patient for Reversal?

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2017 ACC Expert Consensus Decision Pathway on Management of Bleeding in Patients on Oral Anticoagulants, Volume 70, Issue 24, December 2017

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.

​

Identify a Pacer by Chest X-Ray

29/10/2017

 
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Clinicians are confronted every day with a growing number pacemakers (PMs), implantable cardioverter-defibrillators (ICDs) and implantable loop recorders (ILRs). Collectively these devices are sub summarised as cardiac rhythm management devices (CRMDs). Identification of these devices is simple as long a the patient can present an ID card or some other form of identification. This can become challenging especially in emergencies where such information might not be accessible, and interrogation of the pacemaker becomes a problem.
Using the wrong manufacturer-specific device programmer causes a delay in diagnostic and treatment and can be relevant in these situations.​


​
Techniques to identify a CRMD are following:

- Patient's ID card

- Medical records

- Manufacturers' patient registries (All CRMD manufacturers keep their own in-house registry of patients implanted with their devices and provide 24-hour telephone technical support
​
- Device specific radiopaque alphanumeric codes (ANC)

All these identification techniques have their problems in clinical practice, and so far no other method or algorithm was available to help out in such a dilemma. Sony Jacob et al. have therefore developed and validated the so-called

Cardiac Rhythm Device Identification Algorithm using X-rays (CaRDIA-X, see below)

The study participants using this algorithm showed an overall accuracy of 96.9%. This study was published in 2011 but only now caught our attention.

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​We have tried this algorithm on a few X-rays ourselves and came to the conclusion:

Using the chart is a little challenge itself, but very helpful in most cases! Certainly worth keeping in mind!



Jacob S et al. Heart Rhythm. 2011 Jun;8(6):915-22.

CT is the Key to Clear the Spine in the Intoxicated!

14/8/2017

 
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We just had the discussion again and finally found a good and solid answer to it:

A 19 year old male was transferred to our unit from casualty with a GCS of 10 (E2, V3, M5) secondary to a little bit of... to many drinks. As he was found lying on the ground with no company an unwitnessed fall was considered and a rigid collar applied by paramedics. A c-spine CT-scan in the hospital showed no abnormalities and the patient was transferred to ICU for further treatment... with the rigid collar still in place!

The question soon arose whether it is safe to remove a rigid collar in the intoxicated and dazed patient after a normal c-spine scan or not. Some argued that the patient should also be examined clinically once sober in order to safely evaluate and clear the spine. As always by the way: The rigid collar was removed in ICU and no further problems evolved. 

At that time we just knew it is safe to do so but now we seem to get some excellent evidence supporting this procedure.

Martin et al. have just published a 

prospective multicenter study at 17 centers

in which they analyzed

10191 trauma patients that underwent CT of the c-spine during their primary evaluation (67% male, 83% car accidents or falls, mean ISS 11)

They found that 

the intoxicated cohort had a lower incidence of c-spine injuries

and that

c-spine CT had a sensitivity of 94%, a specifity of 99.5% and a negative predicitve value of 99.9%!
In words this means that a negative CT-result for a patient gives us a very high confidence that this negative result is true!
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Clearing the c-spine by CT-scan in the intoxicated patient is definitely safe, especially when there are no other injuries or history of a high velocity trauma.


Martin MJ et al. J Trauma Acute Care Surg. 2017 Jul 19

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

Contrast-Induced Nephropathy: Preventing Complications That Don't Exist?

22/2/2017

 
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What's the Problem?

Most radiologic exams, especially computed tomography (CT) scans, use iodinated contrast media in order to improve image quality and therefore diagnostic accuracy. The decision on whether to use IV contrast media is also made on the background of pre-existing renal function as the use of these agents has been linked to increased risk of adverse events like: acute kidney injury, initiation of dialysis, renal failure, stroke, myocardial infarction, and death.
-> So called 'contrast-induced nephropathy' or short CIN!

The REAL PROBLEM is that randomising patients to receive or not receive a contrast-enhanced imaging study when indicated is simply not feasible.

- It has been presumed that these agents are a direct cause of acute kidney injury - and therefore dangerous ☠


But, Hold On: Is There Really a Problem?

The causal relationship between the application of IV contrast media and the development of acute kidney injury has recently been questioned - Seriously questioned!

- It is interesting to notice that most of our current understanding of contrast-induced nephropathy derives from arterial angiography studies.

- Also, many studies looking into this problem were performed without any control populations. These investigators obviously assumed that CIN undoubtably exists but did not compare their cohort to patients not receiving contrast media!

Mitchell AM et al. nn Emerg Med. 2015 Sep;66(3):267-274 or Mitchell AM et al. lin J Am Soc Nephrol. 2010 Jan;5(1):4-9. doi: 10 and more!
🤔

- As a matter of fact, serum creatinine level fluctuations (meeting the criteria for contrast induced nephropathy) occur in patients in patients undergoing unenhanced CT at similar rates to those published after contrast-enhanced CT. Newhouse JH et al. (see reference below) for instance looked at a total of over 32'000 patients and noticed that creatinine level increases in patients who are not receiving contrast material as often as it does in published series of patients who are receiving contrast material.

AJR Am J Roentgenol. 2008 Aug;191(2):376-82

Newhouse already suspected that CIN may have been overestimated so far! Also other studies found no increased of acute kidney injury after after contrast media administration in any patient group, regardless of baseline renal function.

Crit Cloud review from March 2014

Crit Cloud review from January 2015
​


Maybe There is No Major Problem

Two recently published paper further challenge the paradigm of contrast-induced nephropathy.

Hinson J et al. published a single-center retrospective cohort study in 2016 in which a total of 17'934 patient visits to their emergency department over a period of 5 years were included. They analysed three patient groups that where demographically similar: contrast-enhanced CT, unenhanced CT and no CT scan performed. In this largest controlled study of it's kind no difference was found in the incidence of acute kidney injury.

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

And just now Wilhelm-Leen et al. have published their analysis of almost 6'000'000 hospitalised patients in the united states and their risk of radio-contrast associated nephropathy. Their results strongly suggest, that the incremental risk of AKI that can be attributed to contrast-media is modest at worst, and almost certainly overestimated!


Wilhelm-Leen Emilee, J Am Soc Nephrol 28: 653-659,2017

A most recent editorial by Lopez-Ruiz at al. puts this new knowledge into a new perspective.

J Am Soc Nephrol. 2017 Feb;28(2):397-399

- If contrast induced nephropathy does exist, it's relevance in clinical practice seems to have been overestimated so far!


Is There a Way to Prevents Contrast-Induced Nephropathy?

The application of sodium bicarbonate, N-acetylcysteine, statins, ascorbic acid and pre-hydration with IV fluids have been recommended for the prevention of CIN in patients with compromised renal function. Among all of these measures hydration with intravenous saline is considered the cornerstone in the prevention of CIN.

And luckily enough just now The Lancet provides us with a first answer to this specific question. The AMAZING trial published in February 2017 provides fairly good evidence that prophylactic hydration with normal saline does not lower the incidence of CIN.

EC Nijssen et al. The Lancet, Feb. 2017


The Bottom Line:

- Until proven otherwise IV contrast media should be considered potentially nephrotoxic. This is supported by preclinical and cardiac studies. If this is relevant in clinical practice (escpecially for CT scans) is not proven so far... but also difficult to disapprove!

- The risk of contrast-induced nephropathy certainly has been oversetimated so far!

​- While prophylactic hydration of the patient has no benefit in regards of CIN, keeping patients well hydrated in general is certainly strongly recommended.

- Quick and proper treatment of the patients underlying condition is most probably more important than worrying about CIN and therefore withholding an indicated enhanced CT-scan!

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

Oxic Hazard?

13/10/2016

 
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Oxygen is life! There is no doubt, a lack of oxygen is no good and can have lethal consequences in humans. The mitochondrial reduction of oxygen sustains life in aerobic organisms and therefore makes oxygen to one of our most used medications in critical care.

The Free Radical Theory

But as important oxygen is to help sustain life, it's excess (hyperoxia) has proven to be actually harmful itself. This post provides a brief insight into this topic including some of the important references.

Oxygen toxicity is attributed to the free radical theory in which the partial reduction of oxygen forms the superoxide anion radical. Superoxide is a toxic free radical with an unpaired valence shell electron in the outer orbital and is one of several free radicals known.

These reactive oxygen species are formed primarily in the mitochondria, but also by neutrophils and endothelial cells and by the conversion of xanthines. The anti-oxidant defence mechanisms on the other hand consist of several enzymes and small molecules (Vit. A, C and E, Coenzyme Q etc.). An imbalance of these reactions leads to oxidative stress resulting in tissue damage.

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Lung Toxicity

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Already back in 1899 J. Lorrain Smith et al. noticed the toxic effect of high oxygen concentrations. It had been observed that "oxygen at a tension of over 100% of an atmosphere produced pneumonia in the normal animal". In their conclusion (at that time called 'General Résumé') they state: "Oxygen which at the tension of the atmosphere stimulates the lung cells to active absorption, at a higher tension acts as an irritant, or pathological stimulant, and produces inflammation". The pulmonary toxicity of oxygen is therefore sometimes still called the 'Lorrain Smith Effect'.

Over the years several investigations have shown the toxic properties of oxygen in mice, primates and also humans. 

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​Gerald Nash et al. finally brought this topic to the level of critical care with an article in the NEJM in 1967. He performed autopsies in 70 patients that had been on mechanical ventilation with high inspired fractions of oxygen. He was able to show that lung damage correlated with the level of FiO2 applied. He also noticed that early changes were mainly oedematous and exudative while the late phase was characterised by fibro-proliferative changes.

Other Implications of Hyperoxia
  • Hyperoxia seems to impair left ventricular function:
            Mak S et al, Chest 2001 Aug;120(2):467-73.
            Haque W et al. J Am Coll Cardiol.
 1996
 Feb;27(2):353-7.

  • The systematic use of supplemental oxygen patients with acute myocardial infarction appears to increase the risk of death:
            Cabello JB et al. Cochrane Database Syst Rev. 2013 Aug 21;(8):CD007160

  • Hyperoxia is associated with increased mortality in patients admitted to the ICU after resuscitation:
           Kilgannon JH, JAMA. 2010 Jun 2;303(21):2165-71​

  • Mean values of FiO2 and PaO2 in the first 24 hours directly correlated with mortality (although it is not clear whether this association is causal or merely a reflection of differences in severity of illness):
            De Jonge et al. Crit Care. 2008;12(6):R156

  • Supplemental oxygen in patients with ST-elevation myocardial infarction but without hypoxia seems to increase early myocardial injury and is associated with larger myocardial infarct size:       
            Stub et al. Circulation. 2015 Jun 16;131(24):2143-50.

Latest News

Another interesting input on this topic comes from Girardi and his team who have published an interesting randomised clinical trial comparing the treatment of ICU patients with either oxygen in a conventional manner or according to a restrictive protocol. In this single-centre study his team have recruited 480 patients with an expected intensive care unit length of stay of 72 hours or longer.
In this interdisciplinary ICU the patients were then randomly assigned to receive oxygen therapy to maintain a Pao2 between 70 and 100 mm Hg (or Spo2 between 94% and 98%, 'conservative group') or, according to standard ICU practice, to allow Pao2 values up to 150 mm Hg (or Spo2 between 97% and 100%, 'conventional control group').
Interestingly, the conservative protocol was associated with an absolute risk reduction for intensive care unit mortality of 8.6% compared with that for patients treated with conventional therapy.

The patient populations were comparable, but still there are some limitations to this study. One of them is that the trial was terminated early due to an earthquake in the region of the hospital. Nevertheless, these findings earn respect.
Take Home Messages

- Oxygen is definitely toxic at high concentrations!

- Oxygen toxicity does not only depend on the concentration of oxygen applied it also depends on the duration of exposure!

What should you do?

- Oxygen is a drug, you need to dose accordingly!

- Keep the FiO2 <0.6 whenever possible... and always at the lowest acceptable

- Current recommendation is to achieve paO2 values of 60-80mmHg (ARDSnet.org)



And Remember:

Never withhold oxygen in an emergency setting, especially when the patient needs it!

​
The Pathological Effects Due to Increase of Oxygen Tension in the Air Breathed, J. Lorrain et al., J. Physiol. 1899;24;19-35

G. Nash et al. N Engl J Med 1967; 276:368-374

Girardis M et al. JAMA. 2016;316(15):1583-1589

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
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