Incredible Case Demonstrating the Value of Frequent Serial ECGs

This case is presented and written by Vince DiGiulio, (EMT-Critical Care and emergency department tech).  As his title shows, he is a tech.  Not a paramedic.  Not a nurse.  Not a doctor.  He is a wizard at reading ECGs and is entirely self-taught.  He was the ECG tech on this case, and his skills mean that he recognized the pathology on the ECG and could stand there and keep recording them.

A 75 year old female presents with a chief complaint of “reflux.” 

Starting about five days ago, a couple of times each day she has experienced a burning sensation behind the lower third of her sternum that is relieved within 10-15 minutes of taking an over-the-counter antacid. She has been diagnosed with GERD in the past and always carries a roll of calcium-carbonate chewables in her purse.

Today she woke with the same pain, but this time it lasted at least an hour before subsiding. A couple of hours later the pain returned, and when it had not diminished after another hour she decided to come to the ED.

The following ECG is captured on arrival, approximately 90 minutes after onset of the latest episode of pain. The pain has been constant and she rates it as a 4/10.


Is this ECG diagnostic of any abnormality? A previous EKG will be available but it will take a few minutes to pull up.



There is a poor R-wave progression across the precordials (transition is between V4 and V5); subtle ST-elevation in V2-V4, I, and aVL; and reciprocal ST-depression in II, III, and aVF. Additionally, using the BER vs. anterior STEMI calculator on the right side of this page, the equation value of this tracing is 25.4, greater than 23.4 (using measurements of 2.7 mm, 400 ms, and 4.4 mm, respectively). This tracing is diagnostic of anterior subepicardial ischemia, almost always due to LAD occlusion.

As the tech running this EKG, at this point I recognized our patient was almost certainly experiencing a STEMI but knew I would have a tough time convincing our emergency physician, let alone the cardiologist. So, wanting to be sure I was getting the best data possible and not seeing a falsely poor R-wave progression due to incorrect precordial electrode placement, I double checked my stickers (that were all fine) and ran a second ECG exactly 90 seconds later…

After only 90 seconds the anterior STEMI is now obvious, enough so that it even triggers the machine’s ***ACUTE MI*** alert.

That’s all it took, 90 seconds, with absolutely no change in patient symptoms or condition, and now we have a clearly diagnostic tracing. At this point the cath lab was activated and we finally had time to pull up the patient’s old ECG.


Here is the patient's basline ECG:
Normal


While preparing the patient for transfer, I kept the patient wired and shot the following tracings:
Only 4 minutes after the first ECG and the ST-elevation keeps growing. Her heart rate has also increased, probably because around this time the doctor was giving the, “I’m concerned about your heart” speech all emergency care providers know so well. 





We’re now 8 minutes after ECG 01 and the ST-elevation in V3 is almost taller than the R-wave.



Watch what happens after Nitroglycerin:

Only minutes after the first SL nitro tablet (0.4 mg) and suddenly the ST/T abnormalities have almost entirely resolved (though the patient is still experiencing the same symptoms). Compared to ECG 01, her anterior T-waves are much more normal in size. The only hints of ischemia are the reciprocal ST- depression in the inferior leads (probably most obvious in aVF) and the upright T-wave in V1, new from her old ECG but very non-specific outside of this scenario. Her equation value is now 23.3, less than 23.4 (using measurements of 1.0 mm, 403 ms, and 5.0 mm).  

Then the T-waves enlarge again!
This ECG is very similar to ECG 05, but worryingly her anterior T-waves have increased in size again. The patient is still symptomatic, although less so, and there are still the same subtle signs of ischemia present as in ECG 05. Of note, her rate has also slowed significantly secondary to 5mg of metoprolol. Her equation value is now 23.8, greater than 23.4 (using measurements of 1.4 mm, 401 ms, and 4.7 mm).



Then after another Nitro:
This tracing is following the second dose of nitro with nearly complete resolution of the patient’s symptoms. Compared to ECG 06, her T-waves have decreased in size again and there seems to be less ST- depression evident in the inferior leads. Even V1 is starting to invert as a return to the patient’s baseline. Outside of the setting of the prior ECG’s, this tracing would be perfectly normal, though there is still some clockwise-rotation of the Z-axis. 

Outcome:

The patient was quickly transferred to the cath lab where a culprit lesion of a large obtuse-marginal artery (surprisingly, it was not LAD, though it would be useful to know more specifics about the coronary anatomy and culprit lesions) was successfully stented with a good outcome. Multi-vessel CAD was also noted, with plans made for CABG sometime after discharge from this hospitalization. After departing the ED, her first troponin-I, drawn eight minutes in at the time of ECG 04, came back at 0.49 ng/mL (ref  is less than 0.04 ng/mL)


There are several important take-home points from this case.

First, the ECG 01 was diagnostic of anterior STEMI right from the start. While there might be a couple of true STEMI mimics that can create this picture (stress cardiomyopathy is the best candidate), in the patient presenting with chest pain, this ECG is their ticket to the cath lab.

Second, acute coronary syndrome and myocardial infarction are incredibly dynamic processes, with vessels occluding, de-occluding, and spasming on a sometimes rapid basis. In this case it took only 90 seconds, with no change in patient symptoms, for her ECG abnormalities to progress from very subtle to markedly  abnormal. Don’t be afraid of serial ECG’s, even if the patient’s symptoms are constant.

Related to that, and this is especially directed towards prehospital providers, don’t ever give nitro without first running a 12-lead. It only took one SL nitro for this patient’s ECG to go from an obvious anterior STEMI in ECG 04 to completely non-diagnostic in ECG 05. If you only had the latter ECG to go on, you would never know that this patient was actually experiencing a true anterior MI. It might not happen too often (see this case: http://hqmeded-ecg.blogspot.com/2011/07/wait-until-after-ecg-to-
give.html), but it’s vitally important information.

Finally, one of the nurses working on this case was shocked when I showed her the rapid changes in the patient’s ST-elevation after the patient had been transferred. She had been closely following the rhythm strip on the three-electrode, three-lead cardiac monitor, and had noticed absolutely no changes or even abnormalities aside from a small amount of ST-depression. This is because she was monitoring lead II, which, if you look back, was equally unimpressive across every ECG I shot. You cannot monitor just a single lead in ACS patients, especially when anterior MI is a concern. These patients need, at the very least, five-electrode cables capable of monitoring the augmented leads along with a chosen precordial lead, if not continuous 12-lead monitoring. As this case demonstrates, the ECG’s of ACS patients can change too rapidly, independent of patient symptoms, to warrant anything less.

Fracture Fridays: Bony complications of repeated shoulder dislocations

The Case

After successfully reducing the shoulder of a young athlete – his fourth, your first. He says the the last 2 times he dislocated it was reduced by his team trainer on the sidelines. You obtain XRays and note the following.

Courtesy of Wikipedia

Courtesy of Wikipedia

The Diagnosis

This is a Bankart lesion. Note the abnormality in the inferior third of the glenoid labrum (in the annotated XRay). With repeated anterior-inferior shoulder dislocations a groove or pocket forms in the front of the glenoid. XRays have sensitivity/specificity in the 60%s with MRI being 96% sensitive and 100% specific according to Cicak et al, J Ultrasound Med, 1998.

Courtesy of Wikipedia

Courtesy of Wikipedia

It is often accompanied by a Hill Sachs lesion, which is a concave cortical depression on the humeral head. The latter is also seen in patients with multiple dislocations, and occurs when the humeral head forcefully impacts against the anteroinferior glenoid rim (seen below).

Courtesy of Wikipedia

Courtesy of Wikipedia

Management

Both of these findings in isolation (or together), and especially in the context of multiple dislocations are basically a signal to send the patient to Ortho. The management of a Hill-Sachs lesion is repair when there is shoulder instability. Bankart lesions are also best managed by a surgeon.

The post Fracture Fridays: Bony complications of repeated shoulder dislocations appeared first on PEM Blog.

Pre-Hospital Furosemide – No, No, Also No

In Ottawa, pre-hospital care includes paramedics authorized to treat acute cardiogenic pulmonary edema in the setting of respiratory distress.  Their treatment, sensibly, includes nitroglycerin.  It also, insensibly, includes furosemide.

Decompensated heart failure, resulting in pulmonary edema and dyspnea, is indeed a sort of fluid overload.  However, these patients frequently are not hypervolemic – they may be euvolemic or even hypovolemic, with other underlying etiologies for decompensation than fluid retention.  This pushes the concept of a strategy for the treatment of acute cardiogenic pulmonary edema with furosemide even further down the nonsense pathway.  Yet, there it is.

This study, a retrospective review of presentations with pre-hospital furosemide administration and hospital diagnoses of acute decompensated heart failure, demonstrates essentially nothing.  The primary outcome was designed to detect serious adverse outcomes associated with furosemide administration, but their comparison groups – furosemide given to heart failure, furosemide given to misdiagnosed heart failure, and furosemide not given to heart failure – are clinically heterogeneous and require probably meaningless adjusted comparisons.  The authors find no significant difference, but this is simply a matter of sample size and study design – a treatment given to a group with no chance of benefit obviously suffers only harms.

Most damning, however, is the utter failure of pre-hospital providers to correctly diagnose heart failure.  Of the 272 cases of heart failure diagnosed on arrival to the ED, pre-hospital providers made the diagnosis in only 110 instances.  Then, pre-hospital providers incorrectly diagnosed an additional 58 cases with heart failure and administered furosemide – when the patient was diagnosed with pneumonia, COPD, or another alternative.

Just say no.

“Prehospital use of furosemide for the treatment of heart failure”

Seizures, Sedation and Saliva

aka Toxicology Conundrum 052

A 21-year-old male with a background of schizophrenia and previous intentional overdose, weighing 70kg, was brought to the ED via ambulance after having a witnessed seizure at home. Prior to this, he was witnessed to be drowsy and salivating excessively by his family but was able to admit to taking 2000mg (20 x 100mg) of his own clozapine an hour prior to his witnessed seizure. His family reported that he did not have access to any other medications as he was ‘closely supervised’ at home. After initially found to be drowsy, he subsequently had a generalised tonic-clonic seizure lasting five minutes. On arrival, paramedics found him to be unresponsive but protecting his airway and sitting up intermittently but non-purposefully. He was tachycardic (130 beats/min) and hypotensive (80mmHg systolic), the latter of which responded to an intravenous fluid bolus of 0.9% saline (1000mL). He had a subsequent seizure en route but this resolved spontaneously. ECG demonstrated a sinus tachycardia with a manually measured QRS and QT durations of 80 ms and 320 ms respectively.

Questions

Q1. What type of drug is clozapine and what receptors does it act on?

Clozapine is an atypical anti-psychotic agent.

Clozapine is commonly prescribed for treatment-refractory schizophrenia. Given this indication, it is not often used and is usually administered under supervision so overdose with this drug is rare.

Clozapine is a tricyclic dibenzodiazepine atypical antipsychotic that acts at multiple receptors with antagonism of D1 and D2 as well as serotonin (5HT2), muscarinic (M1), histaminic (H1), peripheral alpha-adrenoreceptors and gamma-aminobutryic acid (GABA) receptors.

Like other anti-psychotics, the observed action of clozapine at multiple receptors also accounts for the clinical presentation seen in overdose.

Clozapine is available as 25, 50, 100 and 200mg tablets in either packets of 28 or 100 tablets.

 

IMage by Fuse809 - click image for source

IMage by Fuse809 – click image for source

Q2. Describe the toxicokinetics of clozapine

Toxicokinetics of clozapine:

  • Absorption: Rapidly absorbed following oral administration. Intoxication occurs within 4 hours of ingestion.
  • Distribution: Moderate volume of distribution (0.5-3L/kg). Highly protein-bound.
  • Metabolism: Metabolised in the lliver by oxidation (cytochrome P450 1A2, 2D6) to its metabolites with significant first pass effect.
  • Excretion: Mainly in the urine and faces as metabolites

Q3. What are the clinical features of clozapine overdose?

Clozapine, like many other anti-psychotics, has multiple potential toxicological properties owing to its actions at multiple receptors. Toxicity usually resolves within 24 hours.

Effects include:

CNS effects

  • Lethargy, confusion, sedation, coma (the latter requiring intubation is rare)
  • Seizures occur in ~5-10% of patients
  • Extra-pyramidal side-effects are more common in children

Cardiovascular effects

  • Sinus tachycardia, hypotension (due to alpha2-adrenoreceptor blockade)
  • QT prolongation is rare

Anti-muscarinic effects

  • Agitation, restlessness, delirium, mydriasis (big pupils) but often have miosis (small pupils due to alpha-bloackade), dry, warm skin, tachycardia, ileus, urinary retention (don’t forget an IDC with an agitated patient post overdose with an anticholinergic!)

Hypersalivation is a characteristic and seemingly paradoxical effect of clozapine toxicity. The mechanism is poorly understood and likely multifactorial

Q4. The patient’s family are adamant he could have not taken anything else. The medical student shadowing you asks if that means you don’t need to order a paracetamol level?  What is your response?

There are two tests that are incredibly useful in Toxicology (not only my opinion but that of many smarter people too):

  1. ECG
  2. paracetamol level

Whilst some patients present to the Emergency Department whilst conscious and clearly volunteer how much and what they have taken, many do not (as in this case). Paracetamol poisoning is often clinically silent initially and, if not treated, can lead to serious morbidity or even mortality. However, it is easily detected via a simple blood test, and has a safe and effective antidote that is widely available. Similarly, the ECG is a cheap, useful non-invasive test useful for identifying otherwise occult cardiotoxicity.

On arrival to the ED, the patient is taken into a resuscitation cubicle. The patient has another episode of hypotension (80/40mmHg) and is given another litre of 0.9% saline. The assist button is pressed thirty minutes later. You race in to find the patient seizing. The seizure is terminated with some midazolam but you notice that the patient is still hypotensive with a blood pressure of 75/40mmHg. What are you going to do?

Q4. What is the risk assessment for this patient?

Whilst clozapine overdose is usually considered to be benign and any accompanying hypotension can be resolved with intravenous fluids alone, this patient has significant hypotension despite adequate filling.

As clozapine is known to act as a peripheral alpha-adrenoreceptor antagonist, commencing an inotrope is suggested. Noradrenaline, an alpha-agonist, is the preferred choice. Alternatives could include other alpha-adrenergic agents such as metaraminol or phenylephrine. In refractory cases, vasopressin has been used with good effect in a previous published case report.

Q5. Whilst the noradrenaline is being hung, your super keen medical student suggests getting an ‘Echo’ because ‘this might be clozapine myocarditis….I read about this once!’. Is it?

Both agranulocytosis and myocarditis are known complications of chronic therapeutic clozapine use, however they are not features of acute overdose.

An echocardiogram may be appropriate if there were concerns about response to inotropes in the setting of hypotension.

Q6. In general, what is the management of clozapine overdose?

Using the Resus-RSI-DEAD approach as all good toxicologists do…

Resuscitation

  • Attention to airway, breathing and circulation always takes precedent. Basic resuscitative measures ensure a good outcome in the vast majority of patients.
  • Treat seizures with benzodiazepines
  • If intravenous fluid does not improve hypotension, consider the use of an inotrope (noradrenaline is generally preferred)

Supportive care and monitoring

  • Supportive care will suffice for most cases so ensure it is done well!
  • Secure appropriate IV access
  • Ensure adequate hydration with IV fluids
  • Remember FASTHUGS IN BED Please especially pressure care, bladder care and DVT prophylaxis
  • Cardiac monitoring should continue until toxicity is reversed if ECG changes are present

Investigations

  • ECG, paracetamol and blood glucose levels should be performed as recommended for all intentional overdoses
  • Consider possible co-ingestants

Decontamination

  • Clozapine is rapidly absorbed and usually benign. Activated charcoal is therefore not indicated on these grounds.

Antidotes

  • None available

Enhanced elimination

  • Not useful

Disposition

  • Haemodynamically stable patients that are symptomatic (i.e. drowsy) can be managed as inpatients in an appropriate ward (e.g. observation unit) until medically cleared (awake, able to walk, has passed urine independently and has tolerated oral intake)
  • Patients requiring inotropic support require HDU/ICU but this is likely to be for a short period of time (~24 hours)
  • Psychiatric review and possible inpatient management

References

Journal articles and Textbooks

  • Burns MJ. The pharmacology and toxicology of atypical antipsychotic agents. J Toxicol Clin Toxicol. 2001;39(1):1-14. Review. PubMed PMID: 11327216.
  • Murray L, Daly FFS, Little M and Cadogan M. Toxicology Handbook (2nd Edition), Elsevier Australia 2011 <Google books preview>
  • Rotella JA, Zarei F, Frauman AG, Greene SL. Refractory hypotension treated with vasopressin after intentional clozapine overdose. European Journal of Emergency Medicine March 17th 2014 (published ahead of print)

The post Seizures, Sedation and Saliva appeared first on LITFL.

April Annals Audio posted!

Apologies for the delay, but here it is, better than ever! Highlights:

-Advance directives and EMS cardiac arrests in Oregon: do they agree?
-Organ donation after cardiac arrest? Ethical and practical issues
-Is outpatient ED care profitable?
-Reimbursement effect of the ACA
-A Standardized Mortality Rate for EM
-Bells Palsy in the ED: how often do we have it right?
-Does it matter which thrombolytic or dose, for ischemic stroke?

And much more…. Email anytime at annalsaudio@acep.org.

D&A

Penicillin for Pneumonia

Penicillin for Pneumonia

Infectious diseases are commonly considered when dealing with pediatric patients.  We have covered topics in this realm numerous times (I believe that this would be the 64th Morsel in the ID category).  One of the more prevalent considerations is pediatric pneumonia.

Previously, we have discussed the issues that surround making the diagnosis of pneumonia.  We have also touched on some complications and interesting pediatric findings.  Additionally, we covered the basic recommended therapies.  While the recommendations are for narrow spectrum antibiotics as 1st line (penicillin), many of us still see a lot of broad spectrum antibiotics being used, particularly for those who we admit to the hospital. While it may be fun to say “Cef-Kill-it-All,” is that the right answer for community acquired pneumonia in children?

 Community Acquired Pneumonia Basics

  • We see a lot of it – accounts for >500,000 ED visits annually!
  • Accounts for ~7% of pediatric admissions.
  • Streptococcus pneumoniae is the most common bacterial cause of community acquired pneumonia in kids.
    • Narrow spectrum beta-lactam antibiotics are still very effective against S. pneumoniae.
    • A significant amount of patients (even after published recommendations) continue to receive unnecessary broad spectrum antibiotics as initial therapy!

 

Penicillin Works Great!

  • Several recent studies (see references) support the fact that narrow spectrum antibiotics for community acquired pneumonia is an effective 1st line option.
    • Penicillin/Ampicillin/Amoxicillin treat uncomplicated community acquired pneumonia as effectively as broad spectrum agents.
    • Broad spectrum antibiotics also work, but increase risk for developing resistant organisms! (Oh, Darwin!)
  • S. pneumoniae is the primary target.
    • Narrow spectrum penicillins provide appropriate coverage for this bug!
    • S. pneumoniae can become resistant to penicillin; however, this is generally a more important consideration for CNS infections (not pneumonia).
  • This is true even for those that you are admitting to the hospital!
    • The adage “Go Big or Go Home,” does not apply to the selection of 1st line antibiotics for community acquired pneumonia!
    • Even if your patient is not going home… you still don’t need to use the “big gun.”
    • If they are not responding within 48 hours, then the decision to change therapies can be made.

     

The Therapeutic Recommendations

  • In 2011, the Pediatric Infectious Diseases Society and the Infectious Disease Society of America published guidelines for management of community acquired pneumonia.
  • OutPatient
    • Pre-School Age and Fully Immunized
      • 1st Line Therapy – Penicillin or Amoxicillin.
      • Honestly, the majority are viral pathogens.
    • School Age and Fully Immunized
      • 1st line therapy = Penicillin or Amoxicillin.
      • Consider Atypical Pathogens
  • InPatient
    • Fully Immunized Infants – School Aged Kids
      • If local epidemiologic data does not show high level of penicillin resistance, then
        • Ampicillin or Penicillin G
      • If local epidemiologic data shows high level of penicillin resistance, then
        • 3rd Generation Cephalosporin (ceftriaxone or cefotaxime)
      • Consider Macrolide for Atypical Pathogens
    • Not Fully Immunized or with Life-Threatening Infections (ex, Empyema)
      • 3rd Generation Cephalosporin (ceftriaxone or cefotaxime)
      • Vancomycin has not been shown to be more effective for empiric therapy in North America.
      • Vancomycin or Clindamycin should be consider if infection is consistent with S. aureus.

       

     

Moral of the Morsel

Obviously, selection of antibiotics for patients needs to be tailored to the specific individual patient (are they immunocompromised, do they have prior history of resistant organisms, are they not vaccinated, etc); however, the decision to admit the patient does not then mandate that the patient receive broad spectrum antibiotics.  Good old fashion penicillins are appropriate initial selections for the patient with uncomplicated community acquired pneumonia – whether admitted or discharged.

 

References

Ross RK1, Hersh AL, Kronman MP, Newland JG, Metjian TA, Localio AR, Zaoutis TE, Gerber JS. Impact of infectious diseases society of america/pediatric infectious diseases society guidelines on treatment of community-acquired pneumonia in hospitalized children. Clin Infect Dis. 2014 Mar;58(6):834-8. PMID: 24399088. [PubMed] [Read by QxMD]

Queen MA1, Myers AL, Hall M, Shah SS, Williams DJ, Auger KA, Jerardi KE, Statile AM, Tieder JS. Comparative effectiveness of empiric antibiotics for community-acquired pneumonia. Pediatrics. 2014 Jan;133(1):e23-9. PMID: 24324001. [PubMed] [Read by QxMD]

Iroh Tam PY. Approach to common bacterial infections: community-acquired pneumonia. Pediatr Clin North Am. 2013 Apr;60(2):437-53. PMID: 23481110. [PubMed] [Read by QxMD]

Williams DJ1, Hall M, Shah SS, Parikh K, Tyler A, Neuman MI, Hersh AL, Brogan TV, Blaschke AJ, Grijalva CG. Narrow vs broad-spectrum antimicrobial therapy for children hospitalized with pneumonia. Pediatrics. 2013 Nov;132(5):e1141-8. PMID: 24167170. [PubMed] [Read by QxMD]

Ambroggio L1, Taylor JA, Tabb LP, Newschaffer CJ, Evans AA, Shah SS. Comparative effectiveness of empiric β-lactam monotherapy and β-lactam-macrolide combination therapy in children hospitalized with community-acquired pneumonia. J Pediatr. 2012 Dec;161(6):1097-103. PMID: 22901738. [PubMed] [Read by QxMD]

Esposito S1, Principi N. Unsolved problems in the approach to pediatric community-acquired pneumonia. Curr Opin Infect Dis. 2012 Jun;25(3):286-91. PMID: 22421754. [PubMed] [Read by QxMD]

Bradley JS1, Byington CL, Shah SS, Alverson B, Carter ER, Harrison C, Kaplan SL, Mace SE, McCracken GH Jr, Moore MR, St Peter SD, Stockwell JA, Swanson JT, Pediatric Infectious Diseases Society and the Infectious Diseases Society of America. The management of community-acquired pneumonia in infants and children older than 3 months of age: clinical practice guidelines by the Pediatric Infectious Diseases Society and the Infectious Diseases Society of America. Clin Infect Dis. 2011 Oct;53(7):e25-76. PMID: 21880587. [PubMed] [Read by QxMD]

Bradley JS1, Byington CL, Shah SS, Alverson B, Carter ER, Harrison C, Kaplan SL, Mace SE, McCracken GH Jr, Moore MR, St Peter SD, Stockwell JA, Swanson JT, Pediatric Infectious Diseases Society and the Infectious Diseases Society of America. Executive summary: the management of community-acquired pneumonia in infants and children older than 3 months of age: clinical practice guidelines by the Pediatric Infectious Diseases Society and the Infectious Diseases Society of America. Clin Infect Dis. 2011 Oct;53(7):617-30. PMID: 21890766. [PubMed] [Read by QxMD]

Tsarouhas N1, Shaw KN, Hodinka RL, Bell LM. Effectiveness of intramuscular penicillin versus oral amoxicillin in the early treatment of outpatient pediatric pneumonia. Pediatr Emerg Care. 1998 Oct;14(5):338-41. PMID: 9814400. [PubMed] [Read by QxMD]

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