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. 

​

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

​

​
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

​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.
​

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

​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

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!

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.

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.

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:
​
​

​
​- 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!

​

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.

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 

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!)

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!
​

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
​

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.
​

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!

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).

​
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

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.

- 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

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

Current evidence shows that Ketamine... 

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

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

- Preserves laryngeal protective reflexes

- Lowers airway resistance

- Increases lung compliance

- Is less likely to cause respiratory depression

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

Ketamine...

- Might increase pulmonary airway pressure and therefore aggravate pulmonary hypertension

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

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

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

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