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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.
​

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

10/3/2019

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​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)

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Handle an Iatrogenic Pneumothorax - Properly!

16/2/2019

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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
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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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​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
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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
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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?

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​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
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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.

​
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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.
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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
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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


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