The BREACH

Reviews and summaries of the latest Emergency Medicine research papers. We try to cover 10 of the best articles each month. Please visit our website for written summaries and to search past editions: www.the-breach.com

March 3rd, 2020    

YEARS for suspected PE in pregnancy

 

Do you ever get up in the morning and think,

“I wish there was another clinical decision rule (CDR) for suspected PE”?

Or even,

“I wish someone would do another blog post/podcast about PE decision rules!”

 

 

No? Fair enough, neither do I – we already have Wells, PERC, D-dimer, age-adjusted D-dimer after all. But wait! Today’s paper has something new to offer us…

 

It describes the first clinical decision tool for PE that has been validated for use in pregnancy.

 

Why are pregnant women challenging?

 

Pregnant women are usually excluded from CDR studies so we are (rightly) nervous about applying decision rules to them. Clinical details are often of little help:

 

Main clinical signs of PE: breathlessness, leg swelling, tachycardia

 

Features of late pregnancy: breathlessness, leg swelling, tachycardia

 

 

We all know that pregnancy increases the risk of PE (although the risk is actually much greater in the post-partum period), and D-dimer rises as the pregnancy progresses.​[1]​ This means it is difficult to ‘rule out’ PE and so we tend to over-investigate suspected cases.

 

The paper

 

Van der Pol LM, Tromeur C, Bistervels IM, et al. Pregnancy-adapted YEARS algorithm for diagnosis of suspected pulmonary embolism. N Engl J Med. 2019;380(12):1139-1149​[2]​

 

(Yes, I know. It's nearly a year since this was published. But I see that pregnancy-adapted YEARS is still relatively unknown and under-utilised in the ED, so forgive me for bringing attention to it here.)

 

A prospective multi-centre study of pregnant women with suspected PE. Nearly 500 patients from the Netherlands and France were enrolled. The authors applied the pregnancy-adapted YEARS algorithm (see diagram below) to each patient, and followed them up for 3 months to ensure no PEs were missed.

 

The overall incidence of PE was only 4.0% - very low but in line with similar studies. When compared to the hypothetical situation of imaging every patient, the algorithm excluded PE in 65% of 1st trimester, 46% of 2nd trimester, and 32% of 3rd trimester women.

 

Limitations

 

A truly robust study would require every patient to receive the gold standard imaging (CT) for the diagnosis or exclusion of PE, but this is unlikely to be in the best interests of the patients involved. Additionally, the efficient follow-up process of this trial (none were lost) meant that clinically relevant PEs were probably not missed.

 

The bottom line

 

The pregnancy-adapted YEARS algorithm is safe. Using it in low risk patients would lead to a reduction in the number of CTs requested.

 

 

Please tell me about this wonderful algorithm

 

Swaminathan A. Pregnancy-adapted YEARS algorithm for PE - ready for prime time?. 2019. REBEL EM. Available at https://rebelem.com/pregnancy-adapted-years-algorithm-for-pe-ready-for-prime-time/

 

So here it is. We now have a clinical decision rule for PE that has been validated for use in pregnancy!

 

 

More FOAMed on this topic

 

The SGEM: In the Pregnant Years – Diagnosing Pulmonary Embolism

 

REBEL EM: Pregnancy-Adapted YEARS Algorithm for PE – Ready for Prime Time?

 

EM Literature of Note: PE in Pregnancy & YEARS Protocol

 


 

  1. Kline J, Kabrhel C. Emergency Evaluation for Pulmonary Embolism, Part 2: Diagnostic Approach. J Emerg Med [Internet] 2015;49(1):104–17. Available from: https://www.ncbi.nlm.nih.gov/pubmed/25800524
  2. van der, Tromeur C, Bistervels I, Ni A, van B, Bertoletti L, et al. Pregnancy-Adapted YEARS Algorithm for Diagnosis of Suspected Pulmonary Embolism. N Engl J Med [Internet] 2019;380(12):1139–49. Available from: https://www.ncbi.nlm.nih.gov/pubmed/30893534

 

February 18th, 2020    

Appendicitis: how to avoid unnecessary referrals (the RIFT study)

 

There is no consensus on the best diagnostic pathway for suspected appendicitis. Some people seem to refer every patient with right iliac fossa (RIF) pain to the surgeons; others require guarding and a fever. Many trust in their clinical examination (guarding, rebound, percussion tenderness, and Rovsing's, psoas or obturator signs), but studies have shown all these clinical signs to be weak discriminators individually, unless perforation has occurred.​[1]​

 

 

So what?

 

In general, the problem with suspected appendicitis is not underdiagnosis but overtreatment. It has been known for some time that more normal appendices are removed in the UK than most other high-income countries. This is likely due, at least in part, to reduced rates of imaging. A stark illustration of this discrepancy is provided by a 2016 study​[2]​ which compared common practice in the UK vs the Netherlands. Preoperative imaging was obtained in 32.8% of UK cases vs 99.5% of Netherlands cases. Normal appendicectomy rates (NAR) were 20.6% (UK) vs 3.2% (Netherlands).

 

Another reason for the UK's high NAR could be the low utilization of risk scoring tools. A recent international consensus document published by the European Association of Endoscopic Surgery​[3]​ recommended routine clinical risk stratification for all cases of suspected appendicitis (they suggested the Alvarado score). Low risk patients should be discharged with safety netting, high risk patients should be worked up for surgery, and intermediate risk patients should have imaging, usually in the form of ultrasound.

 

Scoring systems are not currently recommended in the UK, due to lack of familiarity.​[4]​ The NICE Clinical Knowledge Summary is also curiously silent on the use of imaging for suspected appendicitis.

 

 

The paper

 Nepogodiev D, Matthews JH, Morley GL. Evaluation of appendicitis risk prediction models in adults with suspected appendicitis. Br J Surg. 2020;107(1):73-86​[5]​

 

This was a prospective cohort study involving 5,345 patients across 154 UK hospitals - the RIFT study. It's actually the largest ever study of RIF pain in the world! The focus of this paper, the first of several planned data analyses, was to find the best risk stratification model for identifying low risk patients.

 

Inclusion: patients aged 16-45 who were referred by GP or Emergency Medicine to the on-call surgical team with suspected appendicitis

 

Exclusion: pregnant, prior appendicectomy(!), appendicectomy performed but no histology available

 

The study authors spent some time researching all the risk prediction models in the literature, and then used each on the cases from their study to see which performed the best.

 

Results from the data collection

 

Overall, the rate of normal appendicectomy (NAR) was 20%

 

Likelihood of surgery in women: 32%
NAR rate in women: 28%
Rate of confirmed appendicitis in women: 17%

 

Likelihood of surgery in men: 60%
NAR rate in men: 12%
Rate of confirmed appendicitis in men: 49%

 

Performance of risk models

 

In women, the Adult Appendicitis Score (AAS) performed best. Using a cut-off score of 8 or less, the AAS would have correctly assigned 63.1% of patients without appendicitis into the low risk group. Out of all those in the low risk group, only 3.7% would have been false negatives (i.e. actually had appendicitis)

 

In men, the Appendicitis Inflammatory Response Score (AIRS) was best. Using a cut-off score of 2 or less would have placed 24.7% of those without appendicitis in the low risk group. The false negative rate would have been 2.4%.

 

The bottom line

 

The UK has one of the highest rates of normal appendicectomy in the world, and this is particularly high in women (28%).

 

Using the Adult Appendicitis Score (AAS) would reveal many cases to be low risk for appendicitis, thus saving these patients from further workup, referral, imaging and potentially unnecessary surgery.

 

 

What is the Adult Appendicitis Score?

 

Well, it's a combination of the following rather obvious indicators of appendicitis. Collating them together is more sensitive than taking each in isolation...

 

  • Gender
  • Time from symptom onset
  • RIF pain
  • Pain migrated from central abdomen
  • RIF tenderness on examination
  • Guarding
  • White cell count
  • Neutrophil count
  • CRP level

 

AAS is available here
AIRS is available here
A combination tool has been developed by the authors of the study and is available here

 


 

  1. Andersson R. Meta-analysis of the clinical and laboratory diagnosis of appendicitis. Br J Surg [Internet] 2004;91(1):28–37. Available from: https://www.ncbi.nlm.nih.gov/pubmed/14716790
  2. van R, Bolmers M, Schreinemacher M, Bemelman W, van G, Pinkney T, et al. Diagnosing acute appendicitis: surgery or imaging? Colorectal Dis [Internet] 2016;18(12):1129–32. Available from: https://www.ncbi.nlm.nih.gov/pubmed/27454191
  3. Gorter R, Eker H, Gorter-Stam M, Abis G, Acharya A, Ankersmit M, et al. Diagnosis and management of acute appendicitis. EAES consensus development conference 2015. Surg Endosc [Internet] 2016;30(11):4668–90. Available from: https://www.ncbi.nlm.nih.gov/pubmed/27660247
  4. NICE (National Institute for Health and Care Excellence). Appendicitis [Internet]. NICE Clinical Knowledge Summaries2015 [cited 2020 Feb];Available from: https://cks.nice.org.uk/appendicitis#!topicSummary
    5. Bhangu A, RIFT Study Group on behalf of the West Midlands Research Collaborative. Evaluation of appendicitis risk prediction models in adults with suspected appendicitis. Br J Surg [Internet] 2020;107(1):73–86. Available from: https://www.ncbi.nlm.nih.gov/pubmed/31797357

February 9th, 2020    

Routine Troponin Testing in the Elderly

Elderly patients presenting to the ED frequently have troponin levels sent at triage. When we later see the patient we are often dismayed to find a slightly elevated level. Why might this happen? Well, any of the following can raise the troponin:

  • Tachycardia
  • Infection
  • Ventricular hypertrophy
  • Background ischaemic heart disease
  • Heart valve disease
  • CKD
  • PE
  • Chemotherapy

But could it be a heart attack?

 

On the one hand, it is true that in geriatrics, "atypical is typical" (Christian Nickel). We've known for some time that an elderly person can have an myocardial infarction (MI) without the typical symptom of chest pain. Data analysis of half a million patients on a national registry in the US​[1]​ found that 33% did not report this symptom. The patients in this group were more likely to be elderly, female and to have diabetes or heart failure. Common symptoms included dyspnoea, fatigue, altered mental status and syncope.

On the other hand, it is likely that routine troponin testing rarely benefits patients. If the history doesn't fit with a possible MI, we find ourselves playing a game with numbers. Patients lose in this game, as they usually have to wait for repeat blood tests and sometimes end up with an unnecessary admission.

But what is the actual frequency of MI among elderly ED patients presenting with nonspecific complaints? What a great question! Today's paper is the first to try and answer it...

The paper

Inclusions, exclusions
A retrospective study of patients aged >65 who presented to the ED of one large hospital over a 6-month period with nonspecific complaints. The following were designated to be 'nonspecific' complaints: weakness, dizziness, lethargy, medical problem, examination requested, failure to thrive, multiple complaints. In the UK this group would certainly include the classic "off legs" and "generally unwell". Each patient had to have a troponin level to be included in the study (of course). Two physicians, blinded to the troponin result, checked each case to ensure no specific or focal complaint was subsequently uncovered in the history.

Definition of ACS
ACS (acute coronary syndrome) was defined as any of the following:
1. A documented ST elevation MI
2. An angiogram showing complete occlusion or stenosis >70%
3. A stress test or echo consistent with inducible ischaemia
4. A troponin rise and fall in a pattern typical of ACS with no other obvious alternative cause

This was assessed by two other physicians, also blinded to the study hypothesis. Patients were followed up for 30 days, via the hospital records and those of the regional database to ensure no MIs were missed.

 

Results
Of the 412 patients in the final analysis, 82 (20%) had at least one elevated troponin. Five patients (1.2%) were determined to have had ACS within 30 days. No one developed ACS after being discharged from hospital.

This is a false positive rate of nearly 20%, and gives a risk of ACS of 1.2% in this group.

Limitations

  • It's a descriptive study with no comparison group
  • The definition of 'nonspecific complaint' is pretty subjective
  • Troponin was sent at the discretion of the physician. This suggests that the 182 patients that didn't have a level sent were considered very low risk for ACS. Not including these cases probably led to an over-estimation of the risk. We'd have a more accurate idea if the policy had been to send troponins of every single patient
  • Four of the five patients diagnosed with ACS only had troponin levels and non-stress echo - this falls short of definitively diagnosing an acute MI. In fact, the treating physicians of two of these patients felt they did not have an MI. Taking these two out reduces the risk to 0.7%
  • The one patient with angiography-proven thrombus also had septic shock and severe hyperkalaemia - i.e. she wasn't someone that could have been discharged with a 'silent' MI

Comments

One may argue that no one wants to miss an MI, and even a rate of 1.2% justifies routine troponin testing in this population. However, there are potential harms associated with this approach. Time in hospital is associated with several adverse effects, including infection, deconditioning and delirium.

 

The bottom line

ACS is very rare in elderly patients presenting with nonspecific complaints, but elevated troponin is not. This study does not support routine testing in this group.

  1. Canto J, Shlipak M, Rogers W, Malmgren J, Frederick P, Lambrew C, et al. Prevalence, clinical characteristics, and mortality among patients with myocardial infarction presenting without chest pain. JAMA [Internet] 2000;283(24):3223–9. Available from: https://www.ncbi.nlm.nih.gov/pubmed/10866870
  2. Wang AZ, Schaffer JT, Holt DB, Morgan KL, Hunter BR. Troponin Testing and Coronary Syndrome in Geriatric Patients With Nonspecific Complaints: Are We Overtesting? Acad Emerg Med [Internet] 2019;6–14. Available from: http://dx.doi.org/10.1111/acem.13766
 

February 2nd, 2020    

Penicillin allergy: usually a myth?

 

So many people have a penicillin allergy, don't they? Studies put the incidence at around 10%.​[1]​ One in every ten people you meet are allergic to penicillin. It it were a disease, it would be one of the commonest, comparable to asthma or diabetes...

 

But penicillin is often the first line antibiotic recommended for infections. Why is this? Is this part of a conspiracy to hurt our patients? Or is penicillin allergy usually a myth?

 

A 2017 meta-analysis estimated that around 95% of those with a documented penicillin allergy are actually able to tolerate the antibiotic.​[2]​

 

Another interesting statistic comes from a paper published in 2007.​[3]​ In the 30 years from 1972 to 2007, around 100 million people in the UK were exposed to oral amoxicillin. The number of deaths due to penicillin anaphylaxis during this period? ... One

 

 

In terms of actual mortality risk, this is something akin to being crushed by a flying cow while you sleep. And the mortality risk of a penicillin allergy pales into insignificance compared to the risk of opening a bottle of champagne (24 deaths per year on average).

 

The paper

 

Today's paper is a review piece looking at the epidemiology and best management of penicillin allergy. The authors explain the dangers of failing to challenge a historical documented allergy and give some great advice on how to do this practically.

 

Shenoy E, Macy E, Rowe T, Blumenthal K. Evaluation and Management of Penicillin Allergy: A Review. JAMA 2019;321(2):188–99​[4]​

 

Why 95% of penicillin allergies are not allergies

 

1. The commonest reaction is a delayed benign rash, likely a type IV hypersensitivity reaction. This type doesn't involve antibodies, and can be called a 'nonallergic' reaction. It may not recur on subsequent exposure to the allergen.

 

2. Even if the reaction was a type I hypersensitivity (IgE-mediated), this appears to wane over time. A study from 2012 estimated that around 80% of patients with this type of reaction became tolerant to the allergen over a decade.​[5]​

 

3. Many of those with documented penicillin allergy never actually had an allergic reaction to penicillin at all, but had a viral rash, intolerance or other cause for their symptoms. A large number of reported reactions are simply not allergic and have been incorrectly labelled as such - nausea, diarrhoea, etc.

 

 

Why having a false label of 'penicillin allergy' is bad for patients

 

1. Penicillin is still the first line antibiotic of choice for many types of infections, including skin, abdomen and chest. A documented penicillin allergy often means patients are given a sub-optimal antibiotic, which may fail to adequately treat their infection

 

2. The antibiotic choices for penicillin-allergic patients often have a larger side effect profile than penicillins. Macrolides in particular are infamous for causing diarrhoea. There is also the risk of Clostridium difficile.

 

3. Patients with a documented penicillin allergy are often given broader-spectrum antibiotics, which serves to increase antimicrobial resistance. This leads to the evolution of 'superbugs' like MRSA, which is not only bad for your particular patient but for humanity as a whole...

 

 

What to do about it

 

The authors suggest the following...

 

If your patient has a low risk history, perform a 'Direct Amoxicillin Challenge' - give them a 500mg tablet of amoxicillin and observe them for one hour. The absence of symptoms after this time demonstrates penicillin tolerance (i.e. no allergy).

 

What is a low risk history?

 

  • Itch without rash
  • Gastrointestinal symptoms
  • Other non-allergic symptoms (emotions, dizziness, pain, etc)
  • Family history of penicillin allergy only (no personal experience)
  • History of remote or unknown reaction (over 10 years ago)

 

I think these would cover most of our patients! A direct challenge could be safely performed in the ED, while waiting for other test results. The patient's GP can then be informed, and this allergy can be removed from their file. It's important to do this because patients carry the label of 'penicillin allergy' throughout their lives and, as I sometimes tell patients: "Penicillin might save your life one day."

 

 

How about patients with more severe reactions?

 

Those with a 'moderate risk' history (urticarial rash, swelling or other features of IgE-mediated hypersensitivity) should be referred for skin testing followed by amoxicillin challenge. This obviously cannot be done during a visit to the Emergency Department, but could be suggested to the patient as an option they may not be aware of.

 

For those with a 'high risk' history (anaphylaxis), referral can be made to a Immunologist, who may elect to offer desensitization in a controlled environment. Personally, I tend to just believe patients when they tell me they nearly died after taking penicillin once! I am happy to prescribe a different antibiotic in these cases.

 

 

What about children?

 

In children, less time has passed since their 'penicillin reaction' and so it is often easier to find out what exact features they had.

 

Parents may feel strongly that we should not question their child's allergy, because they have seen a rash with their own eyes. As mentioned above, however, a label of 'penicillin allergy' will follow this child for the next 70 years and so it is important to get it right.

 

Also, as anyone who has worked in paediatrics known, children get rashes all the time, most of which are viral exanthems.

 

A penicillin challenge could certainly be considered in most cases. A 2016 study of 818 children with documented penicillin allergy found that 94% of them were able to tolerate a provocation challenge and could have the allergy label removed from their records.​[6]​

 


 

  1. Zhou L, Dhopeshwarkar N, Blumenthal K, Goss F, Topaz M, Slight S, et al. Drug allergies documented in electronic health records of a large healthcare system. Allergy [Internet] 2016;71(9):1305–13. Available from: https://www.ncbi.nlm.nih.gov/pubmed/26970431
  2. Sacco K, Bates A, Brigham T, Imam J, Burton M. Clinical outcomes following inpatient penicillin allergy testing: A systematic review and meta-analysis. Allergy [Internet] 2017;72(9):1288–96. Available from: https://www.ncbi.nlm.nih.gov/pubmed/28370003
  3. Lee P, Shanson D. Results of a UK survey of fatal anaphylaxis after oral amoxicillin. J Antimicrob Chemother [Internet] 2007;60(5):1172–3. Available from: https://www.ncbi.nlm.nih.gov/pubmed/17761735
  4. Shenoy E, Macy E, Rowe T, Blumenthal K. Evaluation and Management of Penicillin Allergy: A Review. JAMA [Internet] 2019;321(2):188–99. Available from: https://www.ncbi.nlm.nih.gov/pubmed/30644987
  5. Macy E, Ho N. Multiple drug intolerance syndrome: prevalence, clinical characteristics, and management. Ann Allergy Asthma Immunol [Internet] 2012;108(2):88–93. Available from: https://www.ncbi.nlm.nih.gov/pubmed/22289726
  6. Mill C, Primeau M, Medoff E, Lejtenyi C, O’Keefe A, Netchiporouk E, et al. Assessing the Diagnostic Properties of a Graded Oral Provocation Challenge for the Diagnosis of Immediate and Nonimmediate Reactions to Amoxicillin in Children. JAMA Pediatr [Internet] 2016;170(6):e160033. Available from: https://www.ncbi.nlm.nih.gov/pubmed/27043788

 

January 23rd, 2020    

Hanging and strangulation: how to manage in the ED

 

Hanging isn't a super-common presentation to the ED. When it happens, though, there is often some confusion as to how to investigate and manage the patient. Does everyone need a CT? What kind of CT? How can we tell who is high risk for injuries? And what injuries are we looking for anyway?

 

 

Judicial hangings

 

First, a word about classification. There are technically two kinds of 'hanging': judicial and non-judicial. In the ED we rarely see injuries from judicial hangings, because the person in question would not generally survive to hospital. The combination of careful knot placement directly below the occiput and a sudden drop equivalent to the person's height accounts for the mechanism of injury: forceful distraction of the cervical spine, complete cord transection and death.

 

 

Non-judicial hangings and strangulation

 

The pathophysiology in non-judicial hangings (and strangulation) is quite different, and being aware of it will help us to understand the types of injuries to look for. The mechanism of injury is as follows. Sustained pressure on the neck leads to compression of the jugular veins, which are quite superficial, and this obstructs cerebral outflow. The resulting stagnant hypoxia leads to loss of consciousness in as little as 15 seconds. When this happens, muscle tone decreases and the weight of the patient is placed more fully on the neck.

 

Death in such cases is usually the result of arterial occlusion and hypoxic brain injury. Interestingly, external compression of the pharynx and trachea requires a lot of force and is not thought to play a significant role.

 

 

Which injuries are we concerned about?

 

Cervical spine fractures are rare in non-judicial hangings, but the bony, cartilaginous and soft tissue structures of the anterior neck are more vulnerable to injury. These can be categorised in two groups:

 

1. Fractures or contusions of the cricoid, hyoid, laryngeal cartilages or epiglottis. Cricoid fractures in particular can lead to airway obstruction (being the only complete ring), but any of these injuries put the airway at risk because of the resultant bleeding or oedema. Plain radiographs may show subcutaneous emphysema or a hyoid fracture, but CT neck is more sensitive for cartilagenous injuries and should be performed if suspicion is high.

 

2. Blunt vascular injuries. The commonest mechanism for this is compression of the common carotid artery against the transverse processes of C4-6. This can lead to dissection or intramural thrombus. CT angiography (CTA) is the imaging modality of choice for detecting these injuries. Vascular injuries can be missed on regular CT so it's worth actively considering them in every hanging victim as a cognitive forcing strategy.

 

 

What does the literature say?

 

Three recent retrospective studies​[1–3]​ have looked at the incidence of significant injury after hanging / strangulation. An informal pool of their data reveals that out of 552 cases, only 6 had clinically significant injuries. Each of the authors concluded that having a normal GCS and no signs or symptoms of aerodigestive injury (see below) effectively ruled out significant pathology. The low incidence of injury makes me a little cautious about adopting blanket 'rule out' criteria, but these data are certainly reassuring.

 

 

Schberg S, Gupta N, Shah K. Aggressive imaging protocol for hanging patients yields no significant findings: over-imaging of hanging injuries. Am J Emerg Med. 2019;37(4):737-9​[1]​

 

A review of 78 patients, each of which received extensive CT imaging. Only 2 patients had significant findings. One had a sternum fracture with subcutaneous air, and the other had a mild dislocation of the thyroid cartilage, which was reviewed by ENT and required no follow up.

 

Matusz E, Schaffer J, Bachmeier B, et al. Evaluation of nonfatal strangulation in alert adults. Ann Emerg Med. 2019 [epub ahead of print]​[2]​

 

A review of 349 cases of manual strangulation, 60% of whom received advanced imaging. Injuries were identified in 2 cases, both cervical artery dissections. Both of these patients presented with dysphagia.

 

Time for one more study?

 

 

Subramanian M, Hranjec T, Liu L, et al. A case for less workup in near hanging. J Trauma Acute Care Surg. 2016;81(5):925-30​[3]​

 

A review of 125 patients, each of which received extensive CT and MRI imaging. Only 2 significant injuries were found. They found that having a normal GCS and no signs or symptoms of aerodigestive injury effectively ruled out significant pathology.

 

Which clinical features suggest significant injury?

 

The most extensive review of the best evidence-based management of strangulation victims comes from a 2010 paper.​[4]​ The authors suggest that the presence of any of the following features necessitates CT head and neck, with CTA being reserved for those who remain unconscious or have neurological signs...

 

Symptoms

 

  • Reduced level of consciousness on arrival or at scene
  • Breathlessness
  • Dysphagia
  • Hoarse voice

 

Signs

 

  • Erythema or ecchymosis on the neck
  • Any neurological deficit
  • Laryngeal crepitus
  • Facial or conjunctival petechiae

 

This seems as good a list as any to guide our management. Job done!

 


 

  1. Schuberg S, Gupta N, Shah K. Aggressive imaging protocol for hanging patients yields no significant findings: Over-imaging of hanging injuries. Am J Emerg Med [Internet] 2019;37(4):737–9. Available from: https://www.ncbi.nlm.nih.gov/pubmed/30630681
  2. Matusz E, Schaffer J, Bachmeier B, Kirschner J, Musey P, Roumpf S, et al. Evaluation of Nonfatal Strangulation in Alert Adults. Ann Emerg Med [Internet] 2019;Available from: https://www.ncbi.nlm.nih.gov/pubmed/31591013
  3. Subramanian M, Hranjec T, Liu L, Hodgman E, Minshall C, Minei J. A case for less workup in near hanging. J Trauma Acute Care Surg [Internet] 2016;81(5):925–30. Available from: https://www.ncbi.nlm.nih.gov/pubmed/27537511
  4. Stapczynski S. Strangulation Injuries. Emergency Medicine Reports [Internet] 2010;Available from: https://www.reliasmedia.com/articles/19950-strangulation-injuries

 

January 16th, 2020    

Why we shouldn’t fear lactate (that much)

 

 

Lactate... During the last decade it has emerged from obscurity to become the major supervillain of Emergency Medicine.

 

 

 

You may have a colleague who personifies the role of 'lactatologist' in your ED. Every case discussion finishes with the question: "What's the lactate?", whereupon even a slightly elevated level prompts an immediate prescription of an IV fluid bolus. This common knee-jerk response was derided as the 'Lacto-Bolo reflex' by Rory Spiegel in a recent article.​[1]​

 

During some shifts it seems like the management plan for every patient revolves around their lactate. The Observation Ward can become full of patients who are "waiting for their lactate to come down". Well-appearing patients are admitted because their lactate is elevated. In some cases the lactatologist's fear of lactate is so great that a holistic assessment of the patient can take a back seat.

 

 

How did we get here? Should we really be so afraid of lactate? Let's find out...

 

 

The paper

 

Wardi G, Brice J, Correia M. Demystifying lactate in the Emergency Department. Ann Emerg Med. 2019 [epub ahead of print]​[2]​

 

To understand this excellent review article, we need to recap some biochemistry to ensure we are all on the same page. Don't worry, I'll keep it brief...

 

Metabolism is the process by which glucose is converted into ATP molecules, which are subsequently broken down to release energy when needed. There are two pathways that cells can utilise to make ATP from glucose...

 

  1. In well-oxygenated tissues glucose is converted into pyruvate and then acetyl-CoA (glycolysis). This molecule then enters the mitochondria where it is used to produce lots of ATP molecules via the Krebs cycle.
  2. In poorly-oxygenated tissues (e.g. exercising muscle) and cells without mitochondria (e.g. red blood cells), you get a different pathway. Pyruvate is converted to lactate and this is used to produce a few ATP molecules. The lactate then travels to the liver, where it is converted back into glucose (this is called the Cori cycle).

 

 

However (and this is the important bit), this is not an all-or-nothing system. At any given time, some acetyl-CoA is being produced as well as some lactate. Lactate isn't always the harbinger of doom because there are lots of situations that can affect the balance of this equilibrium. This was recognised way back in 1976 when Cohen and Woods​[3]​ categorised lactic acidosis into 2 groups, as follows:

 

Type A: lactate accumulation due to poor tissue perfusion or hypoxia
(shock, major trauma or burns, severe anaemia, mesenteric or limb ischaemia)

 

Type B: lactate accumulation in the absence of poor tissue perfusion or hypoxia
(any other cause - see below)

 

Why almost any patient in the ED can have raised lactate

 

Anything that increases a patient's metabolism can accelerate glycolysis. This causes pyruvate dehydrogenase (PDH - see diagram above) to become saturated, and so relatively more pyruvate is converted into lactate. And there are many, many things that can increase metabolism - increased sympathetic tone, pain, anxiety, salbutamol, adrenaline, infection, etc. A rise in circulating catecholamine leads to elevated lactate via this mechanism - it can be considered a surrogate marker for the physiological 'stress' the body is under.​[4]​

 

 

Other common benign causes of raised lactate

 

Thiamine deficiency: thiamine is a co-factor for PDH, so having reduced stores tips the equilibrium towards less acetyl-CoA and more lactate. This affects alcoholics and malnourished individuals.

 

Liver dysfunction: if a patient's liver function is poor, they will clear lactate less efficiently and so it will accumulate. The same is true, to a lesser extent, of kidney function (around 25% of serum lactate is cleared by the kidneys).

 

Alcohol excess: the process by which ethanol is metabolised to acetate in the liver results in the generation of NADH, which favours the conversion of pyruvate to lactate and inhibits gluconeogenesis.

 

Seizures: the increased muscle activity seen in tonic-clonic seizures results in more anaerobic respiration and therefore lactate production.

 

Hyperventilation: blowing off CO2 results in an alkalosis that then causes a shift of lactate from the intracellular to the extracellular space.​[5]​ Cliff Reid coined the counterintuitive phrase 'lactic alkalosis' to describe this phenomenon - see below for a link to his video.

 

Metformin: inhibits mitochondrial respiration and gluconeugenesis in the liver, both of which contribute to raised lactate levels.

 

Malignancy: patients with cancer often have a raised lactate due to tumour turnover and elevated baseline metabolism, particularly those with haematological malignancies.

 

What about dehydration?

 

One thing that seems NOT to raise the lactate level is dehydration. The reason the 'Lacto-Bolo' reflex often works (in the sense of creating a lower lactate on the post-fluid blood gas) is that we have just diluted the serum lactate. Is the patient better off? Unlikely. Will the lactate return to its elevated level in a few hours? Probably. But... the number is better...

 

 

What about sepsis?

 

Ahhh, sepsis... Just when you thought this post couldn't get any more controversial!

 

Well, we don't want to overstate things. Lactate level does correlate with severity of illness in the septic patient; there is pretty good evidence of its prognostic value in this setting.

 

However, the elevated lactate levels we see in sepsis are unlikely to be caused by tissue hypoperfusion, unless the patient is in persistent shock. In most septic patients, blood flow to the organs is actually increased and the partial pressure of oxygen at the tissue level is normal or even high. In fact, studies have shown that the lungs are a major source of lactate in sepsis​[6]​ - and this lactate is obviously not being produced under anaerobic conditions.

 

The elevated lactate level seen in sepsis is mostly due to endogenous adrenaline stimulation, via the 'accelerated glycolysis' mechanism detailed above. In this sense lactate is useful as a general marker of overall body stress, and this is why it is prognostic. In fact, an interesting ITU study from 2013​[7]​ found that giving beta blockers to patients with septic shock reduced lactate levels, which is what we would expect if the major driver for elevation was sympathetic activation.

 

Take home points

 

1. When confronted with a raised lactate, ask yourself: "Does this patient have signs of regional ischaemia or shock?"

 

2. If not, consider why their lactate might be raised and whether you have to do something about it

 

3. Try to resist the unthinking 'Lacto-Bolo reflex' if you can!

 

More FOAMed on this...

 

RESUS.me - Understanding Elevated Lactate
EMCrit - Understanding Lactate in Sepsis and Using it to our Advantage
EMCrit - iSepsis - the Lactate Myths
St Emlyns - Lactate = LactHATE

 


 

  1. Spiegel R, Gordon D, Marik P. The origins of the Lacto-Bolo eflex: the mythology of lactate in sepsis. J Thorac Dis [Internet] 2019;Available from: http://jtd.amegroups.com/article/view/34647/pdf
  2. Wardi G, Brice J, Correia M, Liu D, Self M, Tainter C. Demystifying Lactate in the Emergency Department. Ann Emerg Med [Internet] 2019;Available from: https://www.ncbi.nlm.nih.gov/pubmed/31474479
  3. Cohen R, Woods H. Clinical and Biochemical Aspects of Lactic Acidosis. Oxford, England: Blackwell Scientific Publications; 1976.
  4. Marik P, Bellomo R. Lactate clearance as a target of therapy in sepsis: a flawed paradigm. OA Critical Care 2013;1:3.
  5. Maddock R. The lactic acid response to alkalosis in panic disorder : an integrative review. J Neuropsychiatry Clin Neurosci [Internet] 2001;13(1):22–34. Available from: https://www.ncbi.nlm.nih.gov/pubmed/11207326
  6. Iscra F, Gullo A, Biolo G. Bench-to-bedside review: lactate and the lung. Crit Care [Internet] 2002;6(4):327–9. Available from: https://www.ncbi.nlm.nih.gov/pubmed/12225608
  7. Morelli A, Ertmer C, Westphal M, Rehberg S, Kampmeier T, Ligges S, et al. Effect of heart rate control with esmolol on hemodynamic and clinical outcomes in patients with septic shock: a randomized clinical trial. JAMA [Internet] 2013;310(16):1683–91. Available from: https://www.ncbi.nlm.nih.gov/pubmed/24108526

 

January 7th, 2020    

Hyperkalaemia: two problems with our current management

 

Problem 1: Too much insulin

 

Insulin is given to patients with abnormally elevated potassium. It works by upregulating the Na-K ATPase pump, so that potassium is moved intracellularly. As a rough guide, the standard dose of 10 units will lower serum potassium by around 1mmol/L. It'll take around 20min to do this and the effect will last for around 4 hours.​[1]​

 

Unfortunately, this therapy carries a significant risk of hypoglycaemia even if the insulin is given with IV dextrose, as is common practice. Two studies from 2019 demonstrated an incidence of hypoglycaemia of around 20%.​[2,3]​

 

Today's paper is interesting because it attempts to quantify this drop in blood glucose, or [BG].

 

The paper

 

Aljabri A, Perona S, Alshibani M, et al. Blood glucose reduction in patients treated with insulin and dextrose for hyperkalaemia. Emerg Med J. 2020;37(1):31-35​[4]​

 

A multi-centre retrospective cohort study of 90 patients with hyperkalaemia. Each received 10 units of IV insulin plus 25g of IV dextrose (equivalent to 50ml of 50% solution). The authors measured the effect of this treatment on [BG]. Here are the results...

 

Median reduction in [BG] 1.3mmol/L (24mg/dL)
Inter-patient variation in [BG] reduction 0.3 - 2.9mmol/L (6 - 53mg/dL)
Incidence of hypoglycaemia
[BG] < 3.9mmol/L (70mg/dL)
22%
Incidence of severe hypoglycaemia
[BG] < 2.2mmol/L (40mg/dL)
6%
Median time to hypoglycaemia 108min

 

The authors found there was a transient increase in [BG] during the first hour, but this was followed by a reduction in subsequent hours. They suggest that the initial protective effects of dextrose are 'outlived' by the exogenous insulin, or overcome by endogenous insulin production in response to the increased [BG].

 

 

So what is the solution to this problem? Well, we could half the dose of insulin. A 2017 paper​[5]​ found this reduced the incidence of hypoglycaemia but didn't affect the reduction in potassium (see our summary here). Another option would be to 'preload' your patient with dextrose before starting insulin if their initial [BG] was low.

 

Take home points

 

1. Treating hyperkalaemia with insulin will cause blood glucose levels to fall, even if you co-administer dextrose

 

2. The drop in blood glucose is highly variable, but may be as much as 2.9mmol/L (53mg/dL)

 

3. The effects of IV dextrose will wear off before those of insulin, so check blood glucose after 1-2 hours

 


 

Problem 2: Too little calcium

 

Hyperkalaemia reduces the resting membrane potential of cardiac myocytes, so they are more likely to spontaneously depolarise. This can result in arrhythmias, of which VF and subsequent cardiac arrest are the worst outcomes. Additionally, hyperkalaemia doesn't usually cause any symptoms - this combination of features make it particularly dangerous. Thus the saying...

 

"The first symptom of hyperkalaemia is death."​[6]​

 

 

Calcium antagonises this effect of potassium on the cardiac myocytes, stabilising the membranes and reducing the risk of arrhythmias. No one really doubts the physiology behind this therapy, but it might surprise you to learn that there have never been RCTs to confirm its efficacy. Additionally, there is apparently no consensus on when calcium should be given and what the best dose is. Thankfully, we have some very sensible advice from the UK Renal Association.​[7]​ Still, in my experience their recommendations are not widely known.

 

 

Before we get to it, and in case you think I'm being a bit of a cowboy with what follows, it's worth bearing in mind that the document was written by...

 

  • 4 consultant nephrologists
  • 3 consultant anaesthetists
  • 1 consultant in acute medicine

 

And it was fully endorsed by...

 

  • The UK Resuscitation Council
  • The Intensive Care Society
  • The Faculty of Intensive Care Medicine
  • The Society for Acute Medicine
  • The College of Emergency Medicine (we weren't 'Royal' back in 2014!)

 

Are you ready for this?

 

 

Firstly, 10ml of 10% calcium gluconate contains 2.26mmol of ionised calcium. 10ml of 10% calcium chloride contains 6.8mmol. The reason calcium gluconate is preferred in most cases is that there is a risk of tissue necrosis if extravasation occurs, and this preparation is more dilute. The authors recommend that an equivalent dose is given in high-risk hyperkalaemia (i.e. 6.8mmol, which is 30ml of 10% calcium gluconate).

 

Secondly, potential adverse effects of calcium include peripheral vasodilation, bradycardia, hypotension, syncope and arrhythmias. Each of these is quite rare, but the risk is not zero. Therefore, the authors recommend that calcium be reserved for those patients who actually need it - those with ECG evidence of cardiac membrane instability. These would include peaked T waves, prolonged PR interval, flattened P waves, widened QRS complexes, brady- and tachycardias.

 

Thirdly, IV calcium has a relatively short duration of action. In cases of prolonged hyperkalaemia, the ECG should be continuously monitored and we should be ready to repeat the calcium dose in 30-60 minutes if needed.

 

Take home points

 

1. Use 10% calcium gluconate unless you have a central line. Give 3 sequential doses of 10ml until the ECG normalises

 

2. Only give calcium if there are ECG changes associated with hyperkalaemia

 

3. The duration of action is 30-60min, so be ready to repeat the dose if ECG changes reappear

 


 

References

  1. Li T, Vijayan A. Insulin for the treatment of hyperkalemia: a double-edged sword? Clin Kidney J [Internet] 2014;7(3):239–41. Available from: https://www.ncbi.nlm.nih.gov/pubmed/25852882
  2. Jacob B, Peasah S, Chan H, Niculas D, Shogbon N. Hypoglycemia Associated With Insulin Use During Treatment of Hyperkalemia Among Emergency Department Patients. Hosp Pharm [Internet] 2019;54(3):197–202. Available from: https://www.ncbi.nlm.nih.gov/pubmed/31205332
  3. Scott NL, Klein LR, Cales E, Driver BE. Hypoglycemia as a complication of intravenous insulin to treat hyperkalemia in the emergency department. The American Journal of Emergency Medicine [Internet] 2019;209–13. Available from: http://dx.doi.org/10.1016/j.ajem.2018.05.016
  4. Aljabri A, Perona S, Alshibani M, Khobrani M, Jarrell D, Patanwala A. Blood glucose reduction in patients treated with insulin and dextrose for hyperkalaemia. Emerg Med J [Internet] 2020;37(1):31–5. Available from: https://www.ncbi.nlm.nih.gov/pubmed/31653693
  5. LaRue H, Peksa G, Shah S. A Comparison of Insulin Doses for the Treatment of Hyperkalemia in Patients with Renal Insufficiency. Pharmacotherapy [Internet] 2017;37(12):1516–22. Available from: https://www.ncbi.nlm.nih.gov/pubmed/28976587
  6. Glasziou P. Practice corner: the first symptom of hyperkalemia is death. ACP J Club [Internet] 2004;140(2):A13. Available from: https://www.ncbi.nlm.nih.gov/pubmed/15122875
  7. Alfonzo A. Clinical Practice Guideline: Treatment of Acute Hyperkalaemia in Adults [Internet]. UK Renal Association2014 [cited 2020 Jan];Available from: https://renal.org/guidelines/

 

January 2nd, 2020    

Acute severe headache: new recommendations from the USA

A few months ago ACEP (the American College of Emergency Physicians) published an update to their 2008 guideline on headache. It's not a comprehensive statement on headache, but focuses mainly on subarachnoid haemorrhage (SAH).

This statement is important, even for doctors outside the USA, because it is one of the first national guidelines to recommend the following 2 evidence-based practices:

  1. Ottawa SAH rule to risk stratify patients with acute severe headache
  2. Negative CT within 6 hours of headache onset to rule out SAH

The paper

Godwin SA, Cherkas DS, Panagos PD, et al. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with acute headache. Ann Emerg Med. 2019 Oct;74(4):e41-e74​[1]​

Can we use a risk stratification tool?

Level B recommendation: YES

The Ottawa subarachnoid haemorrhage (SAH) rule is recommended as being very sensitive (approaching 100%) and safe for ruling out SAH. The authors do note, however, that the rule is poorly specific (around 20%), so using it indiscriminately will result in over-imaging.

I think of this rule as the PERC of headaches - great for ruling out the diagnosis, rubbish for ruling it in.

The Ottawa SAH rule

It is only to be used on patients with:
1. No neurological deficit, and
2. Headache reached maximum severity within 1 hour of onset

If none of the following features are present, SAH is ruled out:

Mnemonic 1: CT HEAD
Collapse (witnessed LOC)
Thunderclap (pain instantly reaches peak)
Hurt neck
Exertion (onset during)
Age >40
Decreased neck flexion

Mnemonic 2: ANT LEaF
Age >40
Neck pain/stiffness
Thunderclap onset
LOC
Exertion
Flexion decreased

2. Does a normal CT within 6 hours rule out SAH?

Level B recommendation: YES

The authors seemed to have difficulty finding studies that met their strict methodological grading criteria. Their initial 594 articles were whittled down to the following two...

Perry et al (2011)​[2]​ was a prospective cohort study of 3,132 patients with sudden onset non-traumatic headache. Of the 7.7% who had a SAH, none were missed on early scan. CT head within 6 hours had a sensitivity of 100%.

Dubosh et al (2016)​[3]​ was a systematic review and meta-analysis of 8,907 patients. A total of 13 patients had a SAH that was missed on early scan, but 11 of these were from a single study of 55 patients. (Having most of the outliers in one small study makes me wonder how reliable that particular study's results are.) However, even including this trial the meta-analysis still yields a sensitivity of 98.7% for CT within 6 hours. We reviewed this paper on The BREACH here.

Why 6 hours?

Blood appears hyperdense on CT because of its high protein content. Acute bleeds are denser than surrounding brain tissue and so shine white. Over time blood proteins are degraded and absorbed and the blood becomes less dense, eventually becoming indistinguishable from brain tissue - SAH could be 'missed' if too much time elapses. This process is highly variable, taking hours to weeks, but several studies​[4,5]​ have shown that the sensitivity of CT for spotting acute blood starts to decrease at 6 hours.

What about the UK?

So, yes, it's worth bearing in mind that this is an American document and there is no corresponding recommendation from NICE as yet.

However, the SHED study is due to start data collection in a few months. The aim is to collect observational data on a cohort of 10,000 patients across 100 UK sites. This will then be used to attempt to externally validate both the Ottawa SAH rule and a 6-hour CT only rule out strategy

So a bit of caution is needed while we wait for official guidance - I'd make sure your consultants are on board before discharging patients with a negative 6 hour CT.

More FOAMed on this...

FOAMcast - ACEP clinical policy on headache
Journal Feed - Acute headache - ACEP policy statement

St Emlyns - Let's talk about subarachnoid haemorrhage (SAH)
REBEL EM - Does a normal head CT within 6 hours of onset of headache rule out SAH?
EM Literature of Note - Is the 6-hour CT for SAH debate over?
SGEM #134 - Listen to what the British doctors say about LPs post CT for SAH
Emergency Physicians Monthly - LP for subarachnoid hemorrhage: the 700 club
EMbeds - Ottawa SAH rule

References

  1. Godwin SA, Cherkas DS, Panagos PD, Shih RD, Byyny R, Wolf SJ, et al. Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department With Acute Headache. Annals of Emergency Medicine [Internet] 2019;e41–74. Available from: http://dx.doi.org/10.1016/j.annemergmed.2019.07.009
  2. Perry JJ, Stiell IG, Sivilotti MLA, Bullard MJ, Emond M, Symington C, et al. Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study. BMJ [Internet] 2011;d4277–d4277. Available from: http://dx.doi.org/10.1136/bmj.d4277
  3. Dubosh N, Bellolio M, Rabinstein A, Edlow J. Sensitivity of Early Brain Computed Tomography to Exclude Aneurysmal Subarachnoid Hemorrhage: A Systematic Review and Meta-Analysis. Stroke [Internet] 2016;47(3):750–5. Available from: https://www.ncbi.nlm.nih.gov/pubmed/26797666
  4. Edlow JA. Managing Patients With Nontraumatic, Severe, Rapid-Onset Headache. Annals of Emergency Medicine [Internet] 2018;400–8. Available from: http://dx.doi.org/10.1016/j.annemergmed.2017.04.044
  5. Sidman R, Connolly E, Lemke T. Subarachnoid Hemorrhage Diagnosis: Lumbar Puncture Is Still Needed When the Computed Tomography Scan Is Normal. Academic Emergency Medicine [Internet] 1996;827–31. Available from: http://dx.doi.org/10.1111/j.1553-2712.1996.tb03526.x

December 16th, 2019    

How best to screen for delirium?

 

Delirium is common among elderly emergency department patients, being present in around 12% according to one study.​[1]​ Patients with delirium are at increased risk of mortality, falls, prolonged hospital stay and being discharged to a nursing home. Most concerning of all, ED physicians may miss the diagnosis in as much as 80% of cases.​[2]​

 

How can we improve this?

 

The AMTS is a common way to screen for and assess a patient's level of confusion, but it has several disadvantages. It is nearly 50 years old and is rather culturally-specific. It was originally developed for in-patient use and is not validated for assessing delirium. This brings us to our first point...

 

It is more important to identify delirium than dementia in the Emergency Department.

 

An AMTS of 7/10 is of questionable significance without a known baseline. Of course it is useful to know whether your patient has dementia, but it is vital to recognise delirium. Besides all the risks mentioned above, patients with delirium need specific management and support during their admission. There is also a reason that a patient is delirious, and failing to identify delirium often means we don't diagnose the underlying cause.

 

Today's paper is great, because it considers each of the delirium screening tools and offers some evidence as to which ones are best. It also contains a handy review of the major causes of delirium (yes, there's more than just 'infection').

 

The paper

 

Lee S, Gottlieb M, Mulhausen P, et al. Recognition, prevention and treatment fo delirium in emergency department: an evidence-based narrative review. Am J Emerg Med 2019 Oct [epub ahead of print]​[3]​

 

The authors did a comprehensive search of every paper published in English on delirium during the last 23 years, finally arriving at 117 articles. These were read, compared and summarised with the aim of providing an evidence-based review of current delirium management in the ED.

 

What is delirium?

 

Delirium can be called an 'acute confusional state'. It's an episode of mental disorientation that is caused by a physical condition of some sort.​[4]​

 

More exactly, it is defined in DSM-5 (Diagnostic and Statistical Manual of Mental Disorders) as follows:​[5]​

 

  1. Acute onset, fluctuating course (often worse at night)
    and
  2. Reduced ability to focus or sustain attention
    and
  3. Disorganised or incoherent thinking (rambling or illogical flow of ideas)
    or
  4. Altered level of consciousness (lethargic or hyperactive)

 

Screening tools

 

The authors discuss several different tools that have been developed to diagnose delirium. They vary in sensitivity, specificity and administration time. The paper suggests using a brief, sensitive triage tool, to be followed by a slightly more time-consuming, specific diagnostic tool.

 

Triage tools (very sensitive, don't miss any cases)

 

SQiD (single question in delirium):
"Is this person more confused than before?"

 

UB-2 (ultra-brief 2-item bedside test):
"Please tell me the day of the week"
"Please tell me the months of the year backward"

 

DTS (delirium triage screen):
Altered level of consciousness?
"Can you spell the word LUNCH backwards?"

 

Diagnostic tools (very specific, don't over-call delirium)

 

CAM (confusion assessment method):
This asks about each of the features from the DSM-5 definition above. The diagnosis of delirium by CAM requires the presence of features 1 and 2, and either 3 or 4. Most experts recommend that it is administered only by clinicians who have been specifically trained to do so.

 

4AT (4 A's test):
Assigns points to each of the following, more points meaning increased likelihood of delirium. It requires no special training, and can be accessed via MDcalc or the 4AT website.

 

1. Alertness (normal or abnormal)
2. AMT4 (location, age, date of birth, current year)
3. Attention (months backwards)
4. Acute change or fluctuating course

 

A recent study of 785 patients found the 4AT to have a specificity of 94%.​[6]​ SIGN (the Scottish Intercollegiate Guidelines Network) recommend that the 4AT is used to identify patients with probable delirium in the ED.​[6]​

 

The bottom line

 

Rather than concluding that your patient is "a bit confused", actively consider whether they might have delirium. Use the 4AT in patients who are acutely confused, drowsy or agitated.

 

Causes of delirium

 

The authors make three important points about aetiology:

 

  1. Almost any illness can precipitate delirium
  2. Most cases of delirium have more than one cause
  3. Clinicians should not anchor on a UTI as the cause for delirium, as many older patients have pyuria as a baseline

 

A helpful mnemonic for remembering the common causes of delirium is 'PINCH-ME'...

 

 

To these I would add urinary retention (you can think of this as constipation/retention) and electrolytes (under E), as hypercalcaemia in particular is a common cause of delirium.

 


 

More FOAMed on this topic

 

EM3 - Delirium
NUEM - The Seriousness of Deliriousness
emDocs - Delirium

 

References

  1. Baten V, Busch H, Busche C, Schmid B, Heupel-Reuter M, Perlov E, et al. Validation of the Brief Confusion Assessment Method for Screening Delirium in Elderly Medical Patients in a German Emergency Department. Acad Emerg Med [Internet] 2018;25(11):1251–62. Available from: https://www.ncbi.nlm.nih.gov/pubmed/29738102
  2. Lewis L, Miller D, Morley J, Nork M, Lasater L. Unrecognized delirium in ED geriatric patients. Am J Emerg Med [Internet] 1995;13(2):142–5. Available from: https://www.ncbi.nlm.nih.gov/pubmed/7893295
  3. Lee S, Gottlieb M, Mulhausen P, Wilbur J, Reisinger H, Han J, et al. Recognition, prevention, and treatment of delirium in emergency department: An evidence-based narrative review. Am J Emerg Med [Internet] 2019;Available from: https://www.ncbi.nlm.nih.gov/pubmed/31759779
  4. Ahmed Y. Delirium [Internet]. Royal College of Psychiatrists.2019 [cited 2019 Dec];Available from: https://www.rcpsych.ac.uk/mental-health/problems-disorders/delirium
  5. American Psychiatric Association . Diagnostic and statistical manual of mental disorders. 5th ed. Washington DC; 2013.
  6. SIGN . Guideline 157: Risk Reduction and Management of Delirium [Internet]. Scottish Intercollegiate Guidelines Network.2019 [cited 2019 Dec];Available from: https://www.sign.ac.uk/assets/sign157.pdf

 

December 5th, 2019    

Peripheral pressors - what’s the risk?

Background

In May the CENSER trial​[1]​ looked at giving early vasopressors to patients in septic shock. They found that this reduced the time to shock control, risk of pulmonary oedema and mortality at 28 days. We covered this paper on The BREACH - click here.

One potential barrier to adopting this approach in the ED is the perceived need to give vasopressors via a central line. In some hospitals getting central access can be somewhat time-consuming, and may even require conversations with anaesthetics.

But what if you could start a noradrenaline infusion through a good peripheral line? On the one hand, prolonged hypotension and over-administration of IV fluid are bad for your patient. On the other hand, peripheral vasopressors can cause irreversable skin damage if extravasation occurs.

How can we balance these risks? Are both equally risky? This paper strongly suggests they are not. Let's check it out...

The paper

Pancaro C, Shah N, Pasma W, Saager L. Risk of Major Complications After Perioperative Norepinephrine Infusion Through Peripheral Intravenous Lines in a Multicenter Study. Anesth Analg. 2019 Sep [epub ahead of print]​[2]​

A retrospective observational study of 14,385 patients who received noradrenaline via a peripheral line during elective surgery. The paper looked at all cases over a period of 4 years in two Dutch hospitals. The aim was to estimate the risk of complications, in particular skin damage following accidental extravasation.

The noradrenaline was diluted to 20 ug/ml and given at a rate of 40-300 ug/hr, titrated to a satisfactory blood pressure.

There were a total of 5 extravasation events (0.035%). Each had a severity grade of 1, meaning no necrosis, erythema or signs of irritation.

Why is this complication rate so tiny?

The authors put forward the following suggestions:

  1. The anaesthetist was able to monitor the IV site closely and could stop the infusion quickly if extravasation occured. (However I know from experience that anaesthetists do not spend their whole time during surgery staring at a cannula site... How would all those Sudoku puzzles get done?)
  2. The patients were undergoing elective surgery and were not acutely unwell or in profound shock. Their peripheral circulation was therefore able to reabsorb the noradrenaline quickly.

Limitations

Like any retrospective observational study, these results depend to a large extent on the reporting accuracy of the clinicians involved. However, the authors describe a robust system of adverse event reporting, established for many years and involving staff at every level.

Secondly, this study was carried out under different conditions and involved a different patient population to that seen in the ED. It was carried out in one country, where practices and systems may differ considerably from mine or yours.

The bottom line

In this analysis of over 14,000 cases of peripheral norepinephrine infusion, there were only 5 extravasation events and no complications. Peripheral pressors are safe under these conditions.

What can we do to further minimise the risk?

A systematic review in 2015​[3]​ looked at all the cases of extravasation from peripheral vasopressor administration in the literature. They found 318 events, collected mainly from case reports. They found that 95% of the events occured in infusions that had been running for over 4 hours, and that 85% of the events occured in IV lines placed distal to the antecubital fossa.

So, to reduce the risk of extravasation and skin necrosis:

  1. Use a good proximal line
  2. Don't leave it running for ages
  3. Check it frequently


More FOAMed on this

REBEL EM - Peripheral vasopressors: safe or dangerous?
REBEL EM - Mythbuster: administration of vasopressors through peripheral IV access
First 10 EM - Peripheral vasopressors: the myth and the evidence
PulmCrit - Do phenylephrine and epinephrine require central access?
EM Crit - Peripheral vasopressor infusions and extravasation

References

  1. Permpikul C, Tongyoo S, Viarasilpa T, Trainarongsakul T, Chakorn T, Udompanturak S. Early Use of Norepinephrine in Septic Shock Resuscitation (CENSER). A Randomized Trial. Am J Respir Crit Care Med [Internet] 2019;199(9):1097–105. Available from: https://www.ncbi.nlm.nih.gov/pubmed/30704260
  2. Pancaro C, Shah N, Pasma W, Saager L, Cassidy R, van K, et al. Risk of Major Complications After Perioperative Norepinephrine Infusion Through Peripheral Intravenous Lines in a Multicenter Study. Anesth Analg [Internet] 2019;Available from: https://www.ncbi.nlm.nih.gov/pubmed/31569163
  3. Loubani O, Green R. A systematic review of extravasation and local tissue injury from administration of vasopressors through peripheral intravenous catheters and central venous catheters. J Crit Care [Internet] 2015;30(3):653.e9-17. Available from: https://www.ncbi.nlm.nih.gov/pubmed/25669592

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