Clinical Decision Rules Series Part 2: CDR Implementation

Authors: Barry Sheridan, DO (EM Staff Physician and Professor at SAUSHEC) and Brit Long, MD (@long_brit, EM Chief Resident at SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK) & Justin Bright, MD (@JBright2021)

In part 1 of the series, we introduced the potential need for clinical decision rules (CDRs), how they can potentially assist and hurt providers, and most importantly, what makes a CDR clinically helpful.  To catch up before reading part 2, please see part 1 (http://www.emdocs.net/clinical-decision-rules-part-1/). In part 2, we will delve further into CDRs, particularly how to incorporate CDRs into everyday clinical practice.

How should a CDR be incorporated into clinical pathways and clinical practice?

As examined in the last post, good CDRs undergo rigorous development and validation. This is where the rubber meets the road. CDRs can make practice more efficient and improve flow within the ED.

What obstacles are present?

There are often multiple roadblocks to incorporating a CDR into clinical practice. These can be broken into the 1) individual provider and 2) the institution.

  1. Emergency physicians are a rare breed, and many of us do not appreciate suggestions on how to practice. Individual providers vary in many regards: training, knowledge, experience, and gestalt. Workups and treatments can significantly differ among providers.  With CDRs, physicians may be hesitant to apply these rules to their own practice. They may feel the rules are too complex, too difficult to remember, or detract valuable time from patient care. Providers often feel that gestalt or experience is better than rules.
  1. Institutions may have habits or a culture for particular conditions that may make it difficult to apply a rule.  Tradition or consultant availability may color the use of CDRs. Unfortunately, the medico-legal environment or funding can also play a large role in the use, or lack thereof, for CDRs.

How to incorporate a CDR into practice…

First, ensure the CDR itself is useful. Does it apply to your practice and how will it impact your practice? If your practice does not have a moderate to high volume of a particular disease process addressed by the rule, it may not be of any benefit.  Know the inclusion and exclusion criteria used for rule development.  What information will the rule give you?

One-way vs. Two-way Rules

Before we go further, we need to discuss what information a CDR provides, specifically one-way and two-way rules. One-way rules are like PERC. This rule is specifically designed to rule out pulmonary embolism. A positive test is not meant to guide clinical decision-making. Instead, a negative test in a low risk patient can be used to stop further testing. On the other hand, a two-way rule is like the Ottawa Ankle Rule, discussed in Part 1 of the CDR series. Application of this rule directs the provider to either order or not order an X-ray.

Buy-In

Once we know how a rule can be applied and the information provided, then move on to CDR incorporation. First, you need buy-in. If you are in a group practice, discuss how the group would like to practice and then incorporate it into everyday use.  This can streamline the care of a particular group of patients thereby providing consistent, quality care that is easy to reproduce on a day-to-day basis and also defend medico-legally.

Remember to keep it simple… perhaps nominate a champion who will review the literature, the rule, and then combine excerpts into a one or two sheet summary that can be easily followed and stored for use when needed. Discuss the rule at staff meetings or in department notifications.  This reflects the need for visibility. Ensure the rule is known throughout the department by all staff, not just emergency physicians, but your clerks, technicians, nurses, and other departments (such as internal medicine, surgery, and radiology).

Also involve your consultants and get their buy in.  This can ensure that they understand how you practice and what you expect coupled with their particular issues (like how to get follow up, or a particular drug or dosage).

And now for an example…

As an example of institutional implementation of a CDR, our department recently instituted a group practice for low risk chest pain patients.  We incorporated the HEART pathway into our daily practice.  This led to more consistent, streamlined, quality care for our patients and made it easier for all our staff, residents, and nursing to follow a particular group practice.  Gestalt is still incorporated and has its place in this rule, as one size does not fit all, but 90% plus of our patients can appropriately be incorporated into the pathway.

The Nuts and Bolts

HEART Pathway Implementation: All staff physicians were given the relevant literature regarding the HEART Score. As a group we sat down in a risk management forum, and we went through the literature, the Pathway as it will be implemented in this institution, and unanimously agreed to the Pathway (essentially making it a local guideline). The Pathway was further vetted through Cardiology and Internal Medicine to sign off on safety and follow up appointments. A Project Improvement (PI) process was set in place prior to the beginning of the pathway and will be continually tracked. Furthermore, an Institutional Review Board protocol has been accepted to study the pathway in an ambispective research design looking back 2.5 years and going forward 5 years. This will show the before and after data since the pathway was implemented.

The Current State

Approximately 150 patients have been placed in the pathway in the last 3 months. To date, our MACE (Major Acute Coronary Event) is <1%.  Before we implemented this CDR, approximately 46% of these patients would have been admitted to the hospital for ACS rule out; however, with this pathway these patients are able to be safely discharged home from the ED with follow-up. Coronary Computed Tomography Angiography (CCTA) use has decreased with the pathway, going from 40 studies per month to 12 studies per month leading to another saving in resource utilization. HEART is sometimes compared to TIMI and GRACE (older ACS scores), but these measure risk of death for patients with ACS. The TIMI and GRACE scores do not do as well telling who has ACS in the first place (which was the question we really want to ask when we see our chest pain patients).

Once the CDR has been in use, refinement and monitoring of rule use are necessary. Feedback and measuring adherence can be beneficial. Continually discuss and refine rule implementation over time.  No launch of a project goes without some issues that need to be addressed and adjusted.

Remember to stress that clinical gestalt at times may override the rule no matter how supported and researched it may be… after all none of them are 100% sensitive or specific.  Make sure to examine why clinical gestalt was opted for as it may be reasonable to incorporate that in other versions of the rule.

There are many ways to institute a CDR, let alone decide which ones you choose to use.  We opted for high risk and a high volume presenting complaint. This gets back to the applicability of the CDR. Common chief complaints are great targets for implementing a CDR/pathway.

Summary

– CDRs can benefit emergency departments. Target common conditions managed in the ED.

Identify and address potential roadblocks to CDR use including physicians, ED staff, institution, and culture.

– Keep the rule/pathway simple and easy to use.

– Obtain department and consultant buy-in.

– Keep evaluating the pathway and obtain feedback during use.

Tweak the pathway as needed during implementation and use.

 

References/Further Reading

  1. Stiell IG, Bennett C. Impleentation of clinical decision rules in the emergency department. Acad Emerg Med 2007;14:955-59.
  2. Stiell IG. Clinical decision rules in the emergency department. CMAJ 2000;163(11):1465-66.
  3. Green SM. When do clinical decision rules improve patient care? Ann Emerg Med 2013;62:132-35.
  4. Adams ST, Leveson SH. Clinical prediction rules. BMJ 2012;344:d8312 doi: 10.1136/bmj.d8312.
  5. Helman A. Episode 56 The Stiell Sessions: Clinical Decision Rules and Risk Scales. Emergency Medicine Cases. http://emergencymedicinecases.com/episode-56-stiell-sessions-clinical-decision-rules-risk-scales/.
  6. Backus BE, Six AJ, Kelder JC, et al. A prospective validation of the HEART score for chest pain patients at the emergency 2013 Oct 3;168(3):2153-8. http://www.ncbi.nlm.nih.gov/pubmed/23465250.
  7. Backus BE, Six AJ, Kelder JC, et al. Risk Scores for Patients with Chest Pain: Evaluation in the Emergency Department. Current Cardiology Reviews 2011;7(1):2-8. http://www.ncbi.nlm.nih.gov/pubmed/22294968.
  8. Six AJ, Backus BE, Kelder JC. Chest pain in the emergency room: value of the HEART score. Netherlands Heart Journal. 2008;16(6):191-196. http://www.ncbi.nlm.nih.gov/pubmed/18665203.

The post Clinical Decision Rules Series Part 2: CDR Implementation appeared first on emdocs.

ATACH – 2Vérnyomáscsökkentés spontán intracerebrális…



ATACH - 2

Vérnyomáscsökkentés spontán intracerebrális vérzésben


A 2015-ös AHA ajánlás spontán intracerebrális vérzésben  – a korábbi INTERACT vizsgálat eredményei alapján amelyről később szó is lesz – 150 és 220 Hgmm közötti vérnyomás esetén a vérnyomáscsökkentést biztonságosnak tartja (level 1, Class A), sőt javíthatja funkcionális kimenetelt is (Level 2, Class B).


A most bemutatott ATACH - 2 ezt nem tudja megerősíteni.


A vizsgálat az Egyesült Államokban, Németországban és Ázsiában folyt (Japán, Kína, Dél–Korea, Taiwan) 2011 és 2015 között. 1000 beteget vontak be. Már az elején meg kell jegyezni, hogy 1280–at terveztek, de a pozitív eredmények hiányában korábban felfüggesztették a vizsgálatot.


Spontán intracerebrális vérzéses betegeket a tünetek kezdetétől számított 4.5 órán belül vontak be, ha vérnyomásuk 180 felett volt, GCS-e 5-nél job volt és 60ml-nél kisebb hematómájuk volt. Az elsőként választott vérnyomáscsökkentő nicardipin volt, melyet a Chiesi USA and Astellas Pharma szolgáltatott.

A vérnyomást az intervenciós csoportban 110-140 közé csökkentették, míg a kontroll csoportban 140 és 180 közöttit céloztak meg 24 óráig.


A vizsgáltak átlagéletkora 62 év volt, 55% ázsiai, a GCS a betegek felében (55%) 15 volt, a NIHSS median pont 11, 10%-uknak volt 30ml–nél nagyobb hematómájuk.A randomizálást és kezelést végül, ahogy tervezték a tüneteket követő 3 órán belül megkezdték (182, 184 min).

Eredmények
A halál vagy súlyos neurológiai károsodás a kontroll csoportban 37.7%-ban fordult elő, míg intenzív vérnyomás kezelés esetén 38.7%, ami nem volt szignifikáns.

Kisebb arányban fordult elő viszont a hematóma növekedése (18.9% vs 24.4%)

Ráadásul a szövődmények száma magasabb volt az intenzíven kezelt csoportban.

A szövődmények (hogy pontosan mennyire szignifikánsak ezek a szövődmények az még a Supplementary Materialból sem világos):

- Vese: 0.8% vs 0.2%

- Kardiovaszkuláris: 2.2% vs 1.4%

- Agyi Iszkémia 0.8% vs 0%


Összehasonlítva a már említett INTERACT vizsgálattal Az INTERACT-ban:

- alacsonyabb vérnyomású betegeket vontak be (150-220 vs 180 felett)

- később kezdték meg a kezelést (41%-ban 4 órán belül, míg az ATACH-ban az összesnél 4.5 órán belül)

- magasabb volt a vérnyomás az első órában (150 vs 129hgmm)

- több volt a treatment failure (66% vs 12%), ami azt jelenti, hogy a célvérnyomást 2 órán belül nem érték el.

- az INTERACT-ban 3.6% abszolut rizikócsökkenést találtak az intenzív csoportban


A vizsgálat – minden hátulütője ellenére – alapvetően jól megtervezett és végrehajtott randomizált kontroll csoportos vizsgálat. Miért jutott más eredményre, mint a korábbi INTERACT? A különbségek alapján úgy tűnik, hogy magasabb vérnyomást, agresszívebben csökkentettek ebben a vizsgálatban. Ne feledjük, hogy intracerebrális vérzésnél csak az egyik veszély a hematóma növekedése. A vérnyomás csökkentése a hematóma körüli területek perfúziójának csökkenéséhez is vezethet, szekunder iszkémiás károsodást okozva. Hogy pontosan mi is történik, valószínűleg egyénenként és hematómánként is változik és nem nagyon tudjuk mérni vagy vizsgálni. Addig is, nem biztos, hogy 140 alá törekednék.


http://www.nejm.org/doi/full/10.1056/NEJMoa1603460

Otitis Externa

Swimmer's EarSummertime brings many delightful activities that had been left hibernating during the cold winter months. With each activity, however, comes a variety of injuries and illnesses.  Certainly, we are aware of the potential injuries that come with activities like fireworks or skateboarding, but the summertime water activities bring their own unique issues like submersion injuries or C-spine injuries. Swimming can also lead to more minor, yet very annoying issues, like swimmer’s ear.  Let’s take a moment to enjoy a morsel of Otitis Externa:

 

Otitis Externa: Basics

  • Acute Otitis Externa (AOE) is a diffuse inflammation of the external ear canal. [Rosenfeld, 2014]
  • AOE may involve the pinna or the tympanic membrane.
  • AOE is actually a cellulitis of the ear canal skin.
    • In North America, ~98% of acute otitis externa is due to bacterial infection.
    • Most common bacterial causes:
      • Pseudomonas aeruginosa 
      • Staphylococcus aureus 
      • Polymicrobial
    • Fungal infection is uncommon for acute otitis externa, but plays role in chronic otitis externa or in those who have been treated with antibiotics. [Rosenfeld, 2014]
    • The cellulitis can spread and lead to complications.
  • Cause of otitis externa is multifactorial: [Rosenfeld, 2014]
    • Cerumen actually serves a purpose and efforts to remove it can increase risk of infection
    • Skin disorders may create additional debris in canal that supports infection
    • Local trauma to canal (often from cleaning attempts or hearing aids)
    • Exposure to moist environment (ex, humid summer climate or swimming)
      • Bacteria love to hang out in swimming pools and hot tubs!

 

Otitis Externa: Diagnosis

  • AOE is uncommon in children <2 years of age. [Rosenfeld, 2014]
  • Elements of the diagnosis include: [Rosenfeld, 2014]
    • Rapid onset (often within 48 hours) AND
      • Symptoms of ear canal inflammation:
        • Otalgia (often severe) (seen in ~70%)
        • Itching (seen in 60%)
        • Fullness  (seen in ~20%)
        • May also have hearing loss or jaw pain (worse with jaw movement)
      • Signs of ear canal inflammation:
        • Tenderness of the tragus or pinna or both OR
        • Diffuse ear canal edema or erythema or both
        • May have otorrhea, regional lymphadenitis, TM erythema, or even cellulitis of pinna and adjacent skin.
    • Tenderness of the tragus / pinna is often intense, even if visual inspection is underwhelming.

 

Otitis Externa: Ddx

  • Acute otitis media w/ or w/o TM perforation
    • AOM and AOE may both lead to erythema of the TM.
      • Pneumatic otoscopy can differentiate – AOE will still have mobile TM.
    • AOM with perforation will lead to debris in canal and mimic AOE.
      • AOE will have very tender tragus and pinna while AOM w/ perforation often won’t.
  • Malignant / Necrotizing otitis externa
    • Agressive infection
    • Predominantly affects patients with diabetes or other immunocompromised states
    • 90% due to Pseudomonas aeruginosa 
    • Can lead to skull base osteomyelitis and further invade local structures (like the brain).
    • Facial nerve paralysis may be early sign and is more commonly seen early in children vs adult. [Rubin, 1988]
    • Look for granulation tissue on the floor of the canal and at the bony-cartilaginous junction. [Rosenfeld, 2014]
  • Cholesteatoma
    • Typically painless
    • Has alterations of the TM (ex, retraction, granulation tissue, perforation)
    • Need ENT referral for management
  • Furunculosis (infected hair follicle on outer third of ear canal)
  • Viral infections (ex, HSV – Ramsay Hunt syndrome)
  • TMJ syndrome
  • Skin disorders (ex, eczema, seborrhea, psoriasis) that involve the ear canal
  • Contact allergy (ex, nickel allergy from jewelry)

 

Otitis Externa: Treatment

  • Important to assess for factors that alter management strategies:
    • Perforated TM
    • PE tubes
    • Diabetes
    • Immunocompromised states (ex, HIV)
    • Prior radiation therapy
  • Topical Antimicrobials are the main therapy!
    • Initial therapy for uncomplicated AOE is topical antibiotics. [Rosenfeld, 2014]
    • No clinical difference found between various options, although there is cost difference. [Rosenfeld, 2014]
    • Typical course is for at least 7 days.
    • If ear drops do not infuse easily, the patient may require a wick to be placed in the ear canal.
    • If there is a suspected perforated TM or known PE tubes, avoid ototoxic agents!
      • The middle ear does not have keratinized epithelium so drugs can pass through middle ear and into inner ear.
      • Can lead to hearing loss.
      • Need to avoid medicines with low pH, alcohol, aminoglycosides, or the combination drug neomycin/polymxinB/Hydrocortisone.
      • In US, only quinolone drops are approved for middle ear use.
  • Avoid systemic antibiotics [Rosenfeld, 2014]
    • Oral antibiotics play no role in initial management of uncomplicated AOE.
    • If there is extension of cellulitis outside of the canal or concerning host factors, then systemic antibiotics are needed.
    • Malignant/necrotizing otitis externa requires systemic antibiotics and, possibly, anti-fungal medications in addition to surgical debridement.
  • Do not forget analgesics!!
    • The periosteum is very sensitive.
    • NSAIDs to start with.
    • Low dose opiates may be appropriate.
      • Symptoms should improve within 48/72 hrs so prolonged courses of pain medications are not warranted.
    • Topical anesthetic drops:
      • May mask worsening disease, so great care should be taken if using them.
      • Should not be used if PE tube or TM perforation is present/suspected!
  • Reassess in 48 – 72 hours
    • If no improvement in this timeframe, need to evaluate for other diagnoses.

 

References

Rosenfeld RM1, Schwartz SR, Cannon CR, Roland PS, Simon GR, Kumar KA, Huang WW, Haskell HW, Robertson PJ; American Academy of Otolaryngology–Head and Neck Surgery Foundation. Clinical practice guideline: acute otitis externa executive summary. Otolaryngol Head Neck Surg. 2014 Feb;150(2):161-8. PMID: 24492208. [PubMed] [Read by QxMD]

Rosenfeld RM1, Schwartz SR, Cannon CR, Roland PS, Simon GR, Kumar KA, Huang WW, Haskell HW, Robertson PJ. Clinical practice guideline: acute otitis externa. Otolaryngol Head Neck Surg. 2014 Feb;150(1 Suppl):S1-S24. PMID: 24491310. [PubMed] [Read by QxMD]

Rubin J1, Yu VL, Stool SE. Malignant external otitis in children. J Pediatr. 1988 Dec;113(6):965-70. PMID: 3142986. [PubMed] [Read by QxMD]

The post Otitis Externa appeared first on Pediatric EM Morsels.

MEdIC Case: The Case of the Honorary Authorship

authorship journal-articles-canstockphoto3359042-200x300Welcome to season 3, episode 9 of the ALiEM Medical Education in Cases (MEdIC) series! Our team (Brent Thoma, Sarah Luckett-Gatopoulos, Tamara McColl, Eve Purdy, John Eicken, and Teresa Chan) is pleased to welcome you to our online community of practice where we discuss the practice of academic medicine! In this month’s case a junior staff person is unsure of whether or not to include a senior staff on a paper.

MEdIC Series: The Concept

MEdIC: The Case of the Honorary Authorship

by Dr. Brent Thoma

Dr. Keurin was excited for her meeting with her research mentee, Andrei, today. He was a junior emergency medicine resident with a strong interest in research that had just completed his first project! They were just meeting to review the final draft before submission. As she walked into the coffee shop she saw him slumped in his chair, looking a bit dejected. That wasn’t like him at all.

“Hey Andrei, is everything okay?”

He sighed. “I dunno. I just met with Dr. Lee to talk about this whole submission process. You know, which journal we should submit my manuscript to and such.” Dr. Lee was the program’s Research Director and one of the most renowned emergency medicine researchers in the country. She knew that one of the reason’s that Andrei had ranked the program so highly was so that he could work with the illustrious Dr. Lee and he had confided to her in previous meetings that he had been disappointed about their lack of interaction so far in residency.

“Oh, and that didn’t go well?” she asked.

“Well, I dunno. It was the first time that we had discussed the project since I ran into him in the hall at the beginning of the year. You’ll remember that he hadn’t been too impressed with the idea at that time.”

Dr. Keurin remembered. That was actually how she, a much more junior researcher in the Faculty, had come to be Andrei’s mentor. She thought he had a great idea for a research project and had supported it to fruition.

“Anyways, I had met with him to ask for some advice on where we should submit the manuscript and we had a good chat about that. But then he mentioned that I should send it to him to give it a final once over and add him as the senior author. He said that if we added his name it would strengthen the chance of our paper getting published. I was so shocked that I didn’t know what to say. You’ve really mentored me through this project, that should be your spot! But I’m also worried about my future job and research projects if I were to piss him off. What do you think?”

Dr. Keurin pursed her lips. This was putting her in an awkward position. She recalled a similar conversation from when she was a resident. She had just gone along with it because she figured that was how research worked, but it didn’t feel right then and it still doesn’t feel right now. At the same time, it would be horrible for her prospects at her institution to be on Dr. Lee’s bad side. What should she say?

Discussion Questions

  1. What are the requirements for being listed as an author on a manuscript? Does Dr. Lee meet these authorship criteria? How should the authorship order be determined?
  2. How should Dr. Keurin deal with this situation? What advice should she give to Andrei? Should she confront Dr. Lee?
  3. What are some policies that you have seen that are used to protect junior residents and faculty from encountering this problem?

Weekly Wrap Up

As always, we will post the expert responses and a curated commentary derived from the community responses 2 weeks after the case is published.

This time the experts (3 jointly writing a piece from the University of Toronto)

  • Farah Friesen, Lindsay Baker, and Dr. Stella Ng from the University of Toronto’s Centre for Faculty Development
  • Dr. Kerstin De Wit from McMaster University

On July 25, 2016 we will post the expert responses to this case! After that date, you may continue to comment below, but your commentary will no longer be integrated into the curated commentary. That said, we’d love to hear from you, so please comment below!

All characters in this case are fictitious. Any resemblance to real persons, living or dead, is purely coincidental. Also, as always, we will generate a curated community commentary based on your participation below and on Twitter. We will try to attribute names, but if you choose to comment anonymously, you will be referred to as your pseudonym in our writing.

Author information

Teresa Chan, MD

ALiEM Associate Editor
Emergency Physician, Hamilton
Assistant Professor, McMaster University
Ontario, Canada
+ Teresa Chan

The post MEdIC Case: The Case of the Honorary Authorship appeared first on ALiEM.

Time to pace, no time to waste

Here is another post from one of our senior residents - Dr Gayathri Nadarajan.
It is 5am in the resuscitation room. And just when everyone was starting to space out, the nurse brings in a 18-year-old girl on a wheelchair, following a near-syncopal episode. She looked pale, diaphoretic and something didn’t seem quite right.
Presenting Complaint
Diarrhoea, vomiting  and dizziness for 2 days. No actual syncope or seizure like episodes. No fever. No HI and no headache. Has mild abdominal cramping sensation.
Past Medical History
NIL. Certain she is not pregnant
Vitals
BP 100/60     HR-45/min     Temperature- 36.7
Examination
Unremarkable. Abdomen was soft without any guarding or rebound.
ECG shows
Complete heart block
Figure-18-ECG-showing-third-degree-complete-AV-block-and-a-junctional-escape-rhythm

During the consult….
While talking to the patient, her eyes rolled upwards, her body went stiff and she appeared to have a tonic clonic seizure. I couldn’t feel a pulse and the cardiac monitor showed asystole. We immediately started chest compressions. Within a few seconds, she regained consciousness and was shocked to find all of us fussing over her.
Her heart rate was about 40-45. Hence we gave her atropine and prepared for transcutaneous pacing. While preparing for transcutaneous pacing, she had 2 more episodes of brief tonic clonic seizure following a sinus pause. Dopamine was prepared concurrently as the pacing wires were attached to the monitor.
We finally started pacing her and called for a cardiology consult.
That was not the only problem….
In view of the abdominal discomfort in a young girl with syncope, bedside FAST was done, which showed free fluid in the abdomen.
ruq1
Rapid urine HCG was done, which was negative. Hence a GS consult was called for.

Findings and progress
CT scan showed:
  • Moderate ascites
  • Mild diffuse thickening of the large bowel, which is nonspecific and could be associated with non-specific colitis.
  • Gallbladder is distended.
  • Bilateral pleural effusion with associated atelectasis/ consolidation
Troponin:
Her troponin T was 870 ng/L and CK-MB was 39.99.
FBC:
WCC was 15.4
Rest of her bloods were unremarkable and CXR was clear.

Progress
In ED, we concluded that she had symptomatic heart block and the most likely diagnosis was myocarditis. (after ruling out things like drug overdose, pregnancy)
The free fluid in the abdomen could have possibly been due to an inflammatory process such as colitis
In view of the complete heart block with syncope, she needed tranvenous pacing. Hence the cardiology team reviewed her in the ED.
Patient had the transvenous pacing wire inserted and she was admitted under the CGH cardiology team. Inpatient echo was normal. During her stay, family requested for transfer of care to NHC. She is currently recuperating there. She is currently off the transvenous wire and awaiting a pacemaker.

Learning points
  • It is important to check the pulse in patients with a seizure as the seizure could have been the result of hypoxia to the brain from a loss of cardiac output (such as VF/VT/ ventricular pause). This was probably the mechanism of her tonic clonic seizure.
  • Don’t hesitate to pace. When there is significant bradycardia / sinus pauses, indications to pace are:
    • hemodynamic instability (hypotension/ cold, clammy peripheries),
    • altered conscious level
    • syncope
  • Myocarditis can have various cardiac manifestations. Do not forget to include it in our list of differentials.
  • Free fluid in abdomen doesn’t always mean a surgical abdomen / cause. Clinical correlation is important.

Myocarditis in a nutshell (from Life in the Fast Lane)
Possible ECG changes:
  • Sinus tachycardia.
  • QRS / QT prolongation.
  • Diffuse T wave inversion.
  • Ventricular arrhythmias.
  • AV conduction defects.
  • With inflammation of the adjacent pericardium, ECG features of pericarditis can also been seen
Causes:
  • Viral – including coxsackie B virus, HIV, influenza A, HSV, adenovirus.
  • Bacteria – including mycoplasma, rickettsia, leptospira.
  • Immune mediated – including sarcoidosis, scleroderma, SLE, Kawasaki’s disease.
  • Drugs / toxins – including clozapine, amphetamines.