Question Of The Day #17

question of the day
~ Joseph Ciano, USA ~ Leave a comment
qod17

Which of the following is the most likely cause for the patient’s elevated cardiac troponin level in the emergency department?

  • A) Atrial fibrillation with rapid rate
  • B) Patient age
  • C) Sepsis
  • D) Acute coronary syndrome

Elevated cardiac troponin levels, or troponinemia, are one sign that the myocardium may be infarcting or under some type of stressful condition. Cardiac troponin levels are assessed in conjunction with the clinical history, physical exam, EKG, and another laboratory testing in deciding if troponinemia is due to cardiac ischemia or another condition. Conditions associated with elevated cardiac troponin levels include cardiac ischemia (i.e. STEMI, NSTEMI), cardiac contusion, cardiac procedures, congestive heart failure, renal failure, aortic dissection, tachy- or bradyarrhythmias, rhabdomyolysis with cardiac injury, Takotsubo syndrome, pulmonary embolism, acute stroke, myocarditis, sepsis, severe burns, extreme exertion, and other conditions. It is unlikely that this patient had elevated troponin levels from Acute coronary syndrome (Choice D) as her cardiac catheterization results showed no significant occlusive lesions in the coronary arteries. D-Dimer levels do increase with patient age, but cardiac troponin levels do not increase with patient age (Choice B). Sepsis (Choice C) is a cause for elevated troponin levels, but this patient has no clinical signs or sepsis symptoms. Atrial fibrillation with a rapid rate (Choice A) is the most likely cause of this patient’s elevated troponin level. Correct Answer: A 

Want Another Question?

References

[cite]

You may want to read these

Acute Coronary Syndrome – https://iem-student.org/acute-coronary-syndome-acs/ 

Acute Management Of Supraventricular Tachycardias – https://iem-student.org/2020/01/10/acute-management-of-supraventricular-tachycardias/

Deadly ECG Patterns – 5 Can’t Miss ECG Findings – https://iem-student.org/2019/11/22/deadly-ecg-patterns-5-cant-miss-ecg-findings/

Cardiac Monitoring – https://iem-student.org/cardiac-monitoring/

Mindsores

Mindsores
~ Sajan Acharya, Nepal ~ Leave a comment

The patient said he did not care about his stage IV ulcers. He refused antibiotics for chronic osteomyelitis until we gave him opiates. He denied all other non-opiate alternatives. “The patient has an opiate use disorder but also has pain,” said the pain and palliative doctor. In medicine, we try our best to explain all that a patient is experiencing with one diagnosis. A patient suffering from two different diseases as a diagnosis is frowned upon. But here was a seasoned doctor, speaking with his years of precious experience reflected in his white beard and even whiter apron, telling me that the patient I have barely started to present to him, had two diagnoses.

I had taken care of this patient for some days now. In my head, I would associate all the requests he makes, everything he says, and every single complaint he has, to his addiction. “I do not have an opiate use disorder, I have a pain problem!” said the patient as soon as “addiction” was mentioned. The doctor said, “I know you don’t think you have opiate use disorder.” I thought that was clearly mentioned to calm the patient down. Later I would be surprised to know that the doctor actually meant it.

He gave me an ‘overly simplistic heuristic’ that had helped him remember what patients with substance use disorder are going through. “The first time a patient takes a substance, he feels the intended high. The effect remains for a couple times more. As the effect due to the same dose decreases with subsequent exposure, the patient increases the dose to get the intended effect. This seemingly linear relationship is a tricky one. Soon the patient will depend on the substance only to feel okay. Which, let us remind ourselves, the patient felt before starting to take any substance. Hence, many patients with substance use disorder, claiming they do not do it for the high, they do it because they cannot tolerate “normal” without it. Substance use disorder is a complex topic and one that deserves much more effort and attention than is the scope of this conversation but I hope this ignited an enthusiasm to learn more, in you” That night I read some papers on opiate use disorder.

I sometimes wonder if I am not as sensitive to suffering as my patients are. I wonder if what they taught me about signal transduction in my first year of medical school holds true for day-to-day emotions like it held true for addiction’s pathophysiology. The more we are exposed, the more we desensitize. “Being emotional is understandable but unnecessary and unhelpful”, says Sherlock Holmes in one of his many palimpsests. Maybe I was trying to objectively look at this patient of mine. So much so that it did not occur to me that the patient had stage IV ulcers. All I heard was a cry for the high, which, mistake not, was there. But there was something more, something that was hidden to my objective eyes. In focusing my attention on the patient’s mindsores, I was ignoring his very physical and painful bedsores. I dare say Sherlock was wrong. Only emotions can drive passion. People who are so passionate about the pathways and mechanisms of addiction and people who are emotional about the patients’ problems are the ones who we rely upon to solve this tangled problem of pain and addiction. I appeal to you to acknowledge that this is a complex issue. That is the sole intention of this article. And that is the first step in trying to understand and hopefully help patients with multiple sores.

[cite]

Question Of The Day #16

question of the day
~ Joseph Ciano, USA ~ Leave a comment
qod16

Which of the following is the most appropriate next step in management for this patient’s condition?

  • A) Consult general surgery for exploratory laparotomy
  • B) Apply needle decompression of the chest
  • C) Apply Pericardiocentesis
  • D) Order CT scan of chest, abdomen, and pelvis

This patient sustained a penetrating traumatic injury to the left chest and presented to the emergency department with hemodynamic instability (tachycardic and hypotensive). Some differential diagnoses to consider on arrival include tension pneumothorax, cardiac tamponade, aortic injury, or aero-digestive tract injury. Prior to taking a detailed history on any trauma patient, a primary survey should be performed. The goal of the primary survey in a trauma patient is to identify and treat any life-threatening injuries as soon as possible. The primary survey is also known as the “ABCs.” Sometimes it is referred to as the “ABCDEFs.” This acronym stands for Airway, Breathing, Circulation, Disability, Exposure, and FAST exam (How to learn eFAST exam for free). Each letter is addressed and assessed in the order they exist in the alphabet. This creates a methodical, algorithmic approach to assist the practitioner in assessing the trauma patient for life-threatening injuries. The sonographic view shown in this question is the subxiphoid (cardiac) view and demonstrates the presence of free fluid. Free fluid on ultrasound appears black, or “anechoic” and is assumed to be blood in the setting of trauma. The free fluid is highlighted by red stars in the image below. The collapse of the right ventricle is shown by the yellow arrow in the below image.

cardiac tamponade - explained
SS Video 3 Pericardial Tamponade

In conjunction with hemodynamic instability and a history of penetrating chest trauma, this sonographic view strongly supports the diagnosis of cardiac tamponade. Consulting the general surgery team for exploratory laparotomy (Choice A) would be the correct course of action for a patient with hemodynamic instability and free fluid on the other abdominal views of the FAST exam. Needle decompression of the chest (Choice B) would be the correct initial treatment for a tension pneumothorax. The patient described in the case has clear bilateral lung sounds, no tracheal deviation mentioned, normal O2 saturation on room air, and sonographic demonstration of cardiac tamponade. A CT scan of the chest, abdomen, and pelvis (Choice D) would be indicated in this patient if he had normal vital signs and no free fluid on the FAST exam. A pericardiocentesis (Choice C) is the most appropriate next step in the management of this patient with cardiac tamponade to relieve signs of obstructive shock. It should be noted that this procedure has limitations and is not always effective. Pericardiocentesis is a temporizing treatment with pericardiotomy being the definitive therapy. Blood in an acute hemopericardium may clot and be unable to be aspirated with a large-bore needle. The procedure may injure surrounding organs, such as the liver, intestines, or heart itself. Ultrasound-guidance should be used whenever possible to avoid injury to surrounding organs. Emergent thoracotomy to relieve the cardiac tamponade should be performed on any patient with confirmed cardiac tamponade and cardiac arrest in the Emergency Department. Correct Answer: C

References

[cite]

You may want to read these

Pulmonary Embolism – https://iem-student.org/pulmonary-embolism/

Clinical Decision Rules – https://iem-student.org/clinical-decision-rules/

Question of The Day #6 – https://iem-student.org/2020/07/31/question-of-the-day-6/

Oxygenation and Oximetry

Oxygenation and Oximetry
~ Job Guillen, Mexico ~ Leave a comment

Authors: Job Rodríguez Guillén, Chief of Emergency Department. Hospital H+ Querétaro, México. Regina Pineda Leyte Internal Medic, Anahuac Querétaro University, Mexico. 

Introduction

One of the main goals of mechanical ventilation is oxygenation. Both hypoxemia and hyperoxemia must be avoided and the objectives must be individualized according to the clinical situation and comorbidities of each patient. Oxygenation monitoring is possible at the bedside by physical examination (late clinical signs), pulse oximetry (non-invasive continuous monitoring), and arterial blood gas analysis (gold standard for arterial oxygenation analysis).

Determinants of oxygenation

The main determinant of oxygenation is the mean airway pressure (Paw) and the inspired fraction of oxygen (FiO2). Paw is the average pressure to which the lung is exposed during inspiration and expiration mechanical ventilation (Figure 1). Paw improves oxygenation by allowing the redistribution of oxygen from highly compliant alveoli to less compliant alveoli.(1,2)
Oxygenation and Oximetry - figure 1
Figure 1: Mean airway pressure (Paw) is the integral (area under the curve) of pressure and time. PIP: peak inspiratory pressure; PEEP: positive pressure at the end of expiration; Ti: inspiratory time; Te: expiratory time.
According to the determinants of Paw and the relationship between them, there are five different ways to increase it (Figure 2)
Oxygenation and Oximetry - figure 2
Figure 2: Maneuvers to increase the mean airway pressure (Paw). PEEP: positive pressure at the end of expiration. Only maneuvers 3 and 4 are used in clinical practice to increase Paw and improve oxygenation.

The second determinant of oxygenation is Inspired Oxygen Fraction (FiO2). The use of supplemental oxygen at the hospital level is a common practice and a critical element of intensive care in patients with mechanical ventilation for the management of hypoxemia. However, in recent years it has been shown that higher oxygenation is not the goal. (3) In the same way that hypoxemia should be avoided, hyperoxia should be prevented. (4)

Although the FiO2 can be adjusted in ranges of 21% and up to 100% the lowest value required must be set (preferably <60%) to reach the desired oxygen saturation (SO2) target.

Oxygenation monitoring

Pulse oximetry allows non-invasive monitoring of oxygenation (SpO2), it is simple and reliable in many areas of clinical practice. SpO2 has a confidence rate of 95% ± 4%, so readings ranging between 70% and 100% are considered reliable.(5) In patients with mechanical ventilation, the objective is to identify hypoxemia.

It is important to remember that oximeters do not measure arterial oxygen pressure (PaO2), for this reason, they cannot directly diagnose hypoxemia or hyperoxemia (PaO2 <60 mmHg and PaO2> 120 mmHg respectively).(6)  What they do is “estimate” hypoxemia when SpO2 falls <90%, which would correspond to a PaO2 <60 mmHg according to the oxyhemoglobin dissociation curve (Table 1). (7)  However, it must be taken into account that changes in temperature and pH cause changes in this relationship. As the pH increases (alkalosis) or the temperature decreases (hypothermia), the shift of the curve is to the left since hemoglobin binds more strongly with oxygen, delaying its release to the tissues. Acidosis and fever shift the curve to the right as the hemoglobin molecule decreases its affinity for oxygen, facilitating the release of oxygen to the tissues.

Oxygenation and Oximetry - Table 1
Table 1: Estimation of the oxygenation state according to SpO2. SpO2: oxygen saturation by pulse oximetry; PaO2: arterial oxygen pressure.

SpO2 values <70% are not reliable. If necessary, the oxygenation assessment should be supplemented by arterial gas analysis. The arterial oxygen saturation (SaO2) is the oxygen saturation obtained by this test.

Oxygenation Goals

According to the oxyhemoglobin dissociation curve, the goal of oxygen titration is to achieve a PaO2 in the range of 60-65 mmHg or an SpO2 of approximately 90-92%. However, the objectives must be individualized and the current recommendations for oxygen therapy in critically ill patients. (8) are as follows (Table 2).

Table 2: Recommendations for oxygenation by SpO2. O2: oxygen; SpO2: oxygen saturation by pulse oximetry; AMI: Acute myocardial infarction; EVC: Cerebral vascular event; VM: mechanical ventilation; SIRA: Acute respiratory distress syndrome. Some exceptions apply like carbon monoxide poisoning.

It has been suggested that critically ill patients can tolerate lower levels of PaO2 (“permissive hypoxemia”) (9-10), however, studies are limited to make a recommendation to routine clinical practice.

Conclusions

Oxygenation goals should be established once the requirement for mechanical ventilation is indicated according to the clinical condition of each patient and monitoring that these objectives are met. Pulse oximetry allows continuous, non-invasive monitoring at the bedside. It should be remembered that hyperoxemia, as well as hypoxemia, should be avoided.

References

  1. Marini JJ,Ravenscraft SA. Mean airway pressure: physiologic determinants and clinical importance–Part 1: Physiologic determinants and measurements. Crit Care Med. 1992 Oct;20(10):1461-72.
  2. Marini JJ,Ravenscraft SA. Mean airway pressure: physiologic determinants and clinical importance–Part 2: Clinical implications. Crit Care Med. 1992 Nov;20(11):1604-16.
  3. Girardis M, Busani S, Damiani E, et al. Effect of conservative vs conventional oxygen therapy on mortality among patients in an intensive care unit: the Oxygen-ICU Randomized Clinical Trial. JAMA. 2016;316(15):1583-1589.
  4. Bitterman, Haim. “Bench-to-bedside review: oxygen as a drug.” Critical Care1 (2009): 205.
  5. Chan MM,Chan MM, Chan ED. What is the effect of fingernail polish on pulse oximetry?. Chest. 2003 Jun;123(6):2163-4.
  6. Wandrup JH. Quantifying pulmonary oxygen transfer deficits in critically ill patients. Acta Anaesthesiol Scand Suppl 1995;107:37–44
  7. Allen J. Photoplethysmography and its application in clinical physiological measurement. Physiol Meas 2007;28:R1–39
  8. Siemieniuk Reed A C, Chu Derek K, Kim Lisa Ha-Yeon, Güell-Rous Maria-Rosa, Alhazzani Waleed, Soccal Paola M et al. Oxygen therapy for acutely ill medical patients: a clinical practice guideline BMJ 2018;  363 :k4169
  9. Gilbert-Kawai ET, Mitchell K, Martin D, Carlisle J, Grocott MP. Permissive hypoxaemia versus normoxaemia for mechanically ventilated critically ill patients. Cochrane Database Syst Rev 2014;5:CD009931.
  10. Capellier G, Panwar R. Is it time for permissive hypoxaemia in the intensive care unit? Crit Care Resusc 2011;13:139–141.
[cite]

Question Of The Day #15

question of the day
~ Joseph Ciano, USA ~ Leave a comment
qod 15 - pleuritic chest pain

Which of the following is the best course of action to further evaluate for a diagnosis of pulmonary embolism?

  • A) Perform a V/Q scan
  • B) Draw a D-Dimer test
  • C) Perform a CT Pulmonary Angiogram
  • D) Give lorazepam
Pulmonary embolism (PE) is a potentially lethal diagnosis evaluated by a combination of a thorough history, physical exam, and the use of risk stratification scoring tools. The Wells criteria and the PE rule-out criteria (PERC) are two well-accepted risk stratification tools for PE. These criteria are each listed below (Wieters et al., 2020).

Wells’ Criteria for Pulmonary Embolism

CriteriaPoint Value
Clinical signs and symptoms of DVT+3
PE is #1 diagnosis, or equally likely+3
Heart rate > 100+1.5
Immobilization at least 3 days, or Surgery in the Previous 4 weeks+1.5
Previous, objectively diagnosed PE or DVT+1.5
Hemoptysis+1
Malignancy w/ Treatment within 6 mo, or palliative+1
Interpretation
Score >4 = High probability
Score 2–4 = Moderate probability
Score <2 = Low probability

Pulmonary Embolism Rule Out Criteria

All Variables Must Be Present for <2% Chance of PE
Pulse oximetry >94% (room air)
HR <100
No prior PE or DVT
No recent surgery or trauma within prior 4 wk
No hemoptysis
No estrogen use
No unilateral leg swelling
The patient in this clinical vignette would have a Wells score of 1.5 (low risk) due to her persistent tachycardia of unknown etiology. The PERC rule can not be applied to this patient as she is over 50-years-old and has tachycardia. If the patient was low risk on Wells score and meet all the PERC rule criteria, she would have a less than 2% likelihood of her symptoms being due to a PE. It is important to note that only patients with a low-risk Wells score (low pretest probability for PE) can be subjected to the PERC rule. A low-risk Wells score (<2) is investigated with a D-Dimer test (Choice B), while moderate to high-risk Wells scores are investigated with a CT Pulmonary Angiogram (CTPA) (Choice C). A V/Q Scan (Choice A) is not a first-line test for the diagnosis of PE as it is less sensitive than a CTPA scan. Unlike a CTPA scan, a V/Q scan may be nondiagnostic in the setting of lung consolidation, effusions, or other airspace diseases. V/Q scans are second-line tests to CTPA when there are contraindications to a CTPA (i.e., renal failure). Lorazepam (Choice D) is a benzodiazepine that may be helpful in reducing tachycardia, which is secondary to anxiety. However, this therapy does not help further discern if the patient may have a PE. Correct Answer: B 

References

Wieters J, McDonough J, Catral J. Chest Pain. In: Stone C, Humphries RL. eds. CURRENT Diagnosis & Treatment: Emergency Medicine, 8e. McGraw-Hill; Accessed August 17, 2020. https://accessmedicine.mhmedical.com/content.aspx?bookid=2172&sectionid=165059275

Nickson, C. (2019). Pulmonary Embolism. Life in the Fastlane. Accessed on August 17, 2020. https://litfl.com/pulmonary-embolism/

[cite]

You may want to read these

Pulmonary Embolism – https://iem-student.org/pulmonary-embolism/

Clinical Decision Rules – https://iem-student.org/clinical-decision-rules/

Question of The Day #6 – https://iem-student.org/2020/07/31/question-of-the-day-6/

Exercise is Medicine

Exercise is Medicine
~ Brenda Varriano, Canada ~ Leave a comment

Overview

I strongly believe that exercise is medicine. Exercise has been proven to improve cognitive functioning, reduce burnout rates, and support sound mental well-being. However, developing an exercise regimen can be difficult, especially in a demanding academic program such as medicine where time is limited, or after a long shift in the emergency department (ED). Some common barriers to exercise reported in published studies include lack of time and laziness. Though laziness was the term used in these research studies, I prefer fatigue or burnout. Many classmates and colleagues I know, that do not work out, work themselves to the bone, therefore limiting the excess energy available for working out. While I have yet to experience the fatigue of a long ED shift, I have experienced long workdays, and for me, no matter how tired I am, a quick work out can always help me get back into the zone, feel more productive or improve my mood.  

In university students, physical activity has been linked with decreased rates of burn-out, decreased perceived stress, and higher academic performance. As mentioned in my previous post, burnout is not good for physician performance. Burnout can increase the risk of medical errors, and more importantly, reduce the patient-physician experience. Imagine attending an event with a group of friends or colleagues. Would you be drawn to those who are happy, energetic, and lively; or would you rather spend your time with someone who seems so tired and disengaged, someone who keeps asking you to repeat yourself or do not respond to your social cues in an appropriate manner. I would prefer the former, though I have experienced the latter, and do not want to become victim to compassion fatigue because I could not support my own health and wellness. Compassion fatigue, a term I recently learned, is an inability to empathize or show compassion to others due to physical or mental burn out.

Overall, I believe that exercise is important to support one’s health and avoid compassion fatigue or other signs of burnout. However, when it comes to incorporating exercise into your daily routine, there is no one size fits all. The goal of this article is to share three of my favorite styles of exercise, that can be short and effective if done at a proper intensity. At the end of the article, I will have a list of YouTube Channels that provide free workouts, that I am using during COVID-19 as I wait for the gyms to safely open. All these channels have some videos on Tabata, HIIT, and AMRAP training (described below). These can be shared with patients as well, if appropriate, knowing that at times, exercise can be one of the best forms of medicine out there.

Tabata – Named after the Man, the Myth, the Legend

Tabata training is named after the creator, Dr. Izumi Tabata, and his lab, located in Tokyo. Tabata is a specific form of high-intensity interval training. Each exercise (i.e. push-up) is performed for 4 minutes. Within each 4-minute block, the exercise will be performed for 20s with a 10s rest. Overall, the exercise will be performed 8 times in the 4-minute window frame. The workout can be tailored with as many exercises as one wishes. An example of a 16-minute full-body workout can look like the following:

  1. 4 minutes push-ups (20s on – 10s off x8)
  2. 4 minutes of body-weight squats (20s on – 10s off x8)
  3. 4 minutes of sit-ups (20s on – 10s off x8)
  4. 4 minutes of burpees (20s on – 10s off x8)

Don’t forget that exercises always have modifications. For example, if a lunge or squat hurts your knees or your legs are beat after standing in the ED for a long shift, then a wall sit can always be a substitute.

exercise is medicine

HIIT – High-Intensity Interval Training

HIIT often gets mixed up with Tabata training. While they are very similar, HIIT is not as specific as the Tabata framework. HIIT training is similar in which you perform an exercise at a high intensity for a given amount of time followed by a rest period. The rest is important to prevent injury and give your body time to recover from the previous spurt of exercise. There are two ways this can be incorporated:

  1. One exercise at a time (rest in between every single exercise)

For this style of HIIT, you perform one exercise, the work period, and then rest, the rest period. I remember when I used to run or bike, I would start with a 1:2 ratio of work to rest (30 second sprint, 1 minute rest), and slowly work to a 1:1 ratio (30 second sprint, 30 second rest). The example I gave was a form of cardio, but the principles can apply to weights. For example, bicep curl for 2 minutes and rest for 2 minutes. Squat for 30s, rest for 30s.

  1. A series of exercises with rest after the series

In this second form of HIIT, you perform a series of exercises, as shown in the example below, and only rest after completing the entire series. The duration of the exercise time for each exercise is variable, but the entire series is usually the same.

Credit: https://darebee.com/workouts/beginner-hiit-workout.html
Credit: https://darebee.com/workouts/super-hiit-workout.html

AMRAP – As Many Reps as Possible

In AMRAP exercises, you pick one or two exercises and alternate between the two, until the timer tells you it’s time to rest. For example, say you choose squats and lunges (12 reps each) for the exercises, and you pick a 4-minute work period, then you would alternate between 12 squats and 12 lunges until the 4 minutes had passed. You then rest and can repeat with the same two exercises, or two new exercises for as many rounds as you wish. I love this style because you feel like you got an awesome workout in such a short period of time! It was the closest thing I could get to a runner’s high when I couldn’t run, and I could usually do a shorter workout, and feel satisfied. For the timer, I like the website linked below, which allows you to play with the number of intervals and the work/rest periods. The best part is it’s free and provides audio alerts to let you know when the work or rest period is complete. https://fitlb.com/tabata-timer

Here is an example of a workout I put together this summer. After working out, I always found myself to be more productive during the day.

Note: Reverse lunges reduce strain on knee compared to forward. Also, all channels have low impact workout options.

AMRAP #1 (2-minutes each round + 1-minute rest in between; Repeat series #1-8 workout twice)

  1. Air squats
  2. Plank
  3. Reverse lunge left leg
  4. Reverse lunge right leg
  5. Push-ups
  6. Sit-Ups
  7. Calf Raises
  8. Glute bridge

How to increase the intensity of an exercise: 

  1. Increase the number of reps
  2. Increase the speed of an exercise (make sure form is intact)
  3. Add resistance (weights, bands)
  4. Decrease the rest duration
  5. Perform moves that focus on more than one muscle group

Closing Remarks

I hope you learned a bit more about the three styles of exercise described above. They can be done with or without equipment and can be structured based on your goals. I know I would use a quick ten-minute bout of exercise in between a long spurt of studying whenever I would notice my mental fogginess causing careless errors or diminish my quality of work.  

While I encourage exercise as medicine, I also support a healthy mindset; do not hate yourself if you miss a workout, do not hate yourself if a workout is too hard, do not hate yourself if you need to rest. We are all human. Importantly, we are using our time and energy every week in school to study or in the ED to make sure that we can rapidly diagnose, treat and decide what the next steps in a patient care plan are. This takes energy, and so we need to make sure we use exercise to increase our wellbeing, not inch closer to burn out. My mentor, who is an ED physician in Toronto Western, always told me that the moment you don’t have the time or energy to exercise and socialize with loved ones is the moment you are starting to enter burnout territory. 

Finally, inspired by a classmate, I would like my next article to focus on the impact of shiftwork on sleep hygiene and health, in addition to tactics to overcome the detrimental effects of shiftwork on sleep. Send me a message if you want different wellness topics to be discussed. I am always open to feedback. I look forward to learning alongside the iEM community. Happy exercising!

References and Further Reading

  1. Al-Drees A, Abdulghani H, Irshad M, et al. Physical activity and academic achievement among the medical students: A cross-sectional study. Med Teach. 2016;38 Suppl 1:S66-S72. doi:10.3109/0142159X.2016.1142516
  2. Alexandrova-Karamanova, A., Todorova, I., Montgomery, A., Panagopoulou, E., Costa, P., Baban, A., Davas, A., Milosevic, M., & Mijakoski, D. (2016). Burnout and health behaviors in health professionals from seven European countries. International archives of occupational and environmental health, 89(7), 1059–1075. https://doi-org.cmich.idm.oclc.org/10.1007/s00420-016-1143-5
  3. Costa, E. C., Hay, J. L., Kehler, D. S., Boreskie, K. F., Arora, R. C., Umpierre, D., Szwajcer, A., & Duhamel, T. A. (2018). Effects of High-Intensity Interval Training Versus Moderate-Intensity Continuous Training On Blood Pressure in Adults with Pre- to Established Hypertension: A Systematic Review and Meta-Analysis of Randomized Trials. Sports medicine (Auckland, N.Z.), 48(9), 2127–2142. https://doi-org.cmich.idm.oclc.org/10.1007/s40279-018-0944-y
  4. Cuthill, J. A., & Shaw, M. (2019). Questionnaire survey assessing the leisure-time physical activity of hospital doctors and awareness of UK physical activity recommendations. BMJ open sport & exercise medicine, 5(1), e000534. https://doi.org/10.1136/bmjsem-2019-000534
  5. Pereira, E. S., Krause Neto, W., Calefi, A. S., Georgetti, M., Guerreiro, L., Zocoler, C., & Gama, E. F. (2018). Significant Acute Response of Brain-Derived Neurotrophic Factor Following a Session of Extreme Conditioning Program Is Correlated With Volume of Specific Exercise Training in Trained Men. Frontiers in physiology, 9, 823. https://doi-org.cmich.idm.oclc.org/10.3389/fphys.2018.00823
  6. Rao, C. R., Darshan, B., Das, N., Rajan, V., Bhogun, M., & Gupta, A. (2012). Practice of Physical Activity among Future Doctors: A Cross Sectional Analysis. International journal of preventive medicine, 3(5), 365–369.
  7. Vankim, N. A., & Nelson, T. F. (2013). Vigorous physical activity, mental health, perceived stress, and socializing among college students. American journal of health promotion : AJHP, 28(1), 7–15. https://doi-org.cmich.idm.oclc.org/10.4278/ajhp.111101-QUAN-395
  8. Wewege, M., van den Berg, R., Ward, R. E., & Keech, A. (2017). The effects of high-intensity interval training vs. moderate-intensity continuous training on body composition in overweight and obese adults: a systematic review and meta-analysis. Obesity reviews : an official journal of the International Association for the Study of Obesity, 18(6), 635–646. https://doi-org.cmich.idm.oclc.org/10.1111/obr.12532
  9. Wolf MR, Rosenstock JB. Inadequate Sleep and Exercise Associated with Burnout and Depression Among Medical Students. Acad Psychiatry. 2017;41(2):174-179. doi:10.1007/s40596-016-0526-y
[cite]

Question Of The Day #14

question of the day
~ Joseph Ciano, USA ~ Leave a comment
question of the day 14
40.1 - Pneumothorax 1

Which of the following is the most appropriate treatment for this patient’s condition?

  • A) Start anticoagulation
  • B) Perform needle decompression
  • C) Place small-bore chest tube in left chest
  • D) Start IV antibiotics

Anticoagulation (Choice A) would be the proper treatment for pulmonary embolism, NSTEMI/STEMI, and other conditions. This patient is dyspneic and hypoxemic on the exam, but his chest X-ray offers an alternative explanation for his symptoms. IV antibiotics (Choice D) would be helpful for pneumonia and COPD exacerbation, both of which are possible in this patient, but his chest X-ray offers an alternative explanation for his symptoms. Needle decompression of the left chest (Choice B) would be the appropriate initial treatment for a left-sided “tension” pneumothorax. This patient does have a large left-sided pneumothorax, but the X-ray lacks tracheal deviation, mediastinal shift, and left hemidiaphragm flattening, which can be attributed to tension pneumothorax. Most importantly, the patient lacks the hemodynamic instability that defines tension physiology (i.e. hypotension and tachycardia). In addition, the diagnosis and treatment of tension pneumothorax should be made clinically prior to chest radiography. Signs of hemodynamic instability along with tracheal deviation, absent unilateral lung sounds, and a history of trauma all support a diagnosis of tension pneumothorax. The treatment of a tension pneumothorax requires prompt recognition, needle decompression at the 3rd intercostal space at the midclavicular line, and a tube thoracostomy at the 4-5th intercostal space the anterior axillary line. The recommended needle decompression location is recently shifted to 4-5th intercostal space at the mid-anterior axillary line because the studies showed lower success rates in anterior – mid clavicular approach in adults. This patient has a spontaneous left-sided pneumothorax, not a tension pneumothorax. This is likely secondary to his coughing episodes and severe COPD. The treatment for this would be supplemental oxygen and the placement of a small-bore chest tube (i.e. “pig tail) in the left chest. Correct Answer: C. 

References

Smith LM, Mahler SA. Chest Pain. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill; Accessed August 17, 2020. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=219641169

Nickson, C. (2019) Pneumothorax CCC. Life in the Fastlane. Accessed August 17, 2020. https://litfl.com/pneumothorax-ccc/

[cite]

Developing Clinical Research Ethics in the Developing World

Developing Clinical Research Ethics in the Developing World
~ Sarah Bridge, USA ~ Leave a comment

“You are a research fellow working on a clinical trial for cryptococcal meningitis (CM) in Ugandan AIDS patients. If a patient is diagnosed with CM and enrolled in this trial, they receive free care for treatment duration and reimbursement for non-medical expenses. Seventy-five percent of this population lives on less than two dollars per day and cannot afford these costs otherwise. A woman presents with CM symptoms, but after testing her cerebrospinal fluid, she is instead diagnosed with deadly bacterial meningitis. She cannot be enrolled in the trial and is too poor to buy antibiotics. ”

What do you do?

I recently presented this case at a classroom discussion about global health research ethics. When this dying woman’s mother pulled on my lab coat and pleaded for help one day at the government-run Mbarara Regional Referral Hospital (MRRH), where I worked as a clinical research fellow for nearly a year, I did not know what to do, and neither did my peers.

Like many global health-oriented physicians, my career began with short-term medical mission trips as a pre-medical student. However, I found these trips to be self-serving and unsustainable; indeed, the ethical shortcomings of these trips have long been argued because often participants’ benefits outweigh those receiving of their “help.“[1] Thinking research might be a way to develop an ethical global health career, I completed a summer clinical research project in India, which I found more productive and substantial than short-term mission trips. Galvanized by the belief I could change the world through ethical research, I applied for the clinical research fellowship in Uganda.

Ultimately, I found my experience as ethically fraught as the short-term missions I swore to avoid. I am not alone in these sentiments: others have noted that AIDS in Africa has paradoxically been both a source of significant tragedy and significant academic opportunity. Unfortunately, these opportunities are distributed unevenly, producing fresh inequalities. In their efforts to reduce suffering in Africa, some global health researchers have inadvertently capitalized on the intellectual opportunities provided by those same African sufferers.[2]

At MRRH, where the shortages of gloves, saline, and basic medications reflect the hospital’s poverty and its patients, research-based medical care is often the only care people receive. Academic collaborations between western and sub-Saharan African institutions enable African researchers to publish in journals viewed by western audiences. As of 2017, patients presenting to MRRH with tuberculous meningitis or CM were enrolled in American-run clinical trials and treated without charge by experts with effective medications. Western-based surgical teams have improved MRRH’s surgical capacity, where sophisticated procedures are now performed with modern equipment. In 2004, after multinational research programs dedicated to tackling AIDS, tuberculosis, and malaria (ATM) worldwide were launched in the late 1990s, clinics started supplying HIV-positive Ugandans with free antiretrovirals and other services, causing a significant decline in HIV-related mortality.[3]

However, inequities in patient care are apparent in the areas of MRRH that have not yet benefitted from foreign research dollars, particularly the intensive care unit and the emergency department. The two working ventilators in the hospital are usually occupied by neurosurgical patients. Deaths due to trauma and road traffic accidents in Africa cause the loss of more life-years than AIDS and malaria combined [4], which is also true at MRRH. Like the woman in the case above, patients suffering from other non-ATM infectious diseases are sometimes victims of these inequalities at MRRH.
This unequal distribution of research wealth in a resource-limited setting such as MRRH troubles me. At MRRH, often, patient care follows research dollars; when the money runs out, so does the patient care. The Declaration of Helsinki requires control groups to receive the ‘best’ current treatment, not the local one – and while in developed countries the difference between ‘best’ and ‘local’ may be small, in settings like MRRH this difference is profound and may result in severe ethical consequences.[5]

In March of 2018, I watched a presentation by researchers who conducted a CM clinical trial in eastern Uganda, similar to ours at MRRH. A conference attendee voiced concern that the trial had violated the Helsinki Declaration, since many participants in the control group had not received any treatment. The presenter responded that the standard of care treatment for CM at this hospital was often no treatment, because the hospital had nothing to treat its patients. And, in late 2017 when the CM clinical trial at MRRH ended, CM patients there no longer received free treatment.

Uganda is often cited as the success story in sub-Saharan Africa in its efforts to reduce its HIV burden, largely due to funding from large international research programs.[6] But perhaps these trials reveal that acceptance of this ethical relativism in clinical research could result in the exploitation of underserved populations abroad for research programs that could not be performed in the sponsoring country.[5] Researchers must first be aware that conducting clinical research in resource-limited settings may create as many inequalities as it alleviates, particularly where the minimal standard of care for certain conditions is lacking. Secondly, research is often the conduit for medical care for impoverished people, which in turn creates unique ethical issues.

How can we global health researchers mitigate some of these ethical quandaries? I suggest that before embarking on clinical research (particularly in underserved areas), researchers assess their site’s health care needs and risk of patient exploitation, and that teams include medical anthropologists and epidemiologists well-versed in the local population’s health care needs and their receptiveness to clinical research. At MRRH, this was not a requirement of institutional review board approval for studies, so research teams must take this responsibility onto themselves.

Billions of people worldwide have benefitted from the discoveries that clinical research provides. Unfortunately, historically in our quest for valuable intellectual resources, those benefits have sometimes come at the cost of human exploitation. To maximize the benefit of clinical research for all involved, global health researchers must ensure this exciting and evolving field grows in an ethically sound manner.

References

  1. Roberts M. Duffle Bag Medicine. The Journal of the American Medical Association. 2006;295(13):1491-2.
  2. Crane JT. Scrambling for Africa: AIDS, Expertise, and the Rise of American Global Health Science. Ithaca and London: Cornell University Press; 2013.
  3. Wendler D, Krohmal B, Emanuel EJ, Grady C. Why patients continue to participate in clinical research. Arch Intern Med. 2008;168(12):1294–9.
  4. Hulme P. Mechanisms of trauma at a rural hospital in Uganda. Pan Afr Med J. 2010;7:5.
  5. Angell M. The Ethics of Clinical Research in the Third World. N Engl J Med. 1997;337(12):847–9.
  6.  Epidemiological Fact Sheets on HIV/AIDS and Sexually Transmitted Infections: Uganda [Internet]. 2004. Available from: http://data.unaids.org/publications/fact-sheets01/uganda_en.pdf
[cite]

Question Of The Day #13

question of the day
~ Joseph Ciano, USA ~ Leave a comment
qod13

Which of the following is the most appropriate next step in management for this patient’s condition?

  • A) Cardiology consultation
  • B) Discharge home with prompt outpatient follow-up
  • C) Prescribe a benzodiazepine
  • D) Admission for cardiac stress testing

This patient presents to the emergency department after an atypical, brief episode of chest pain. The list of potential diagnoses that may have caused the pain episodes is extensive. The focus of the Emergency Medicine practitioner should not be to determine the diagnosis per say, but rather to be to identify the presence of any life-threatening conditions (i.e. Myocardial infarction, Aortic dissection, Esophageal Rupture, Pulmonary embolism, Tension pneumothorax, Cardiac tamponade, etc.). Many of these serious diagnoses can be evaluated with a detailed history, physical exam, and basic imaging and lab work if needed. Many risk stratification tools have been developed to evaluate the likelihood a patient has chest pain due to Acute Coronary Syndrome. One well-supported tool with international validation is the HEART score tool. The HEART score categorizes a patient as low (0-3), moderate (4-6), or high risk (7-10) for a Major Adverse Cardiac Event (MACE) based on the patient’s history, EKG, age, risk factors, and troponin level. The below chart from Wieters et al. (2020) outlines the HEART score categories and how to make clinical decisions based on a patient’s score.

HEART score for cardiac risk assessment of major adverse cardiac event (MACE).

CategoryScoreExplanationRisk Features
HistoryHigh-risk features
• Middle- or left-sided chest pain
• Heavy chest pain
• Diaphoresis
• Radiation
• Nausea and vomiting
• Exertional
• Relief of symptoms by sublingual nitrates

Low-risk features
• Well localized
• Sharp pain
• Non-exertional
• No diaphoresis
• No nausea and vomiting
Slightly Suspicious 0Mostly low-risk features
Moderately Suspicious+1Mixture of high-risk and low-risk features
Highly Suspicious+2Mostly high-risk features
ECG
Normal0Completely Normal
Non-specific Repolarization Disturbance+1Non-specific repolarization disturbance• Repolarization abnormalities
• Non-specific T wave changes
• Non-specific ST wave depression or elevation
• Bundle branch blocks
• Pacemaker rhythms
• Left ventricular hypertrophy
• Early repolarization
• Digoxin effect
Significant ST Depression+2Significant ST depression• Ischemic ST-segment depression
• New ischemic T wave inversions
Age
<450
45-64+1
≥ 65+2
Risk Factors• Obesity (Body-Mass Index ≥ 30)
• Current or recent (≤ 90 days)smoker
• Currently treated diabetes mellitus
• Family history of coroner artery disease (1st degree relative < 55 year old)
• Hypercholesterolemia

OR

Any history of atherosclerotic disease earn 2 points:
• Know Coroner artery Disease: Prior myocardial infarctions, percutan coronary intervention (PCI) or coronary artery bypass graft
• Prior stroke or transient ischemic attack
• Peripheral arterial disease
No known risk factors0
1-2 risk factors+1
≥ 3 risk factors or history of atherosclerotic disease+2
Initial Troponin
≤ normal limit0
1-3 x normal limit+1
> 3x normal limit+2

Score 0–3 = 2.5 % MACE over next 6 wk: Discharge home
Score 4–6 = 22.3% MACE over next 6 wk: Admit for observation
Score 7–10 = 72.7% MACE over next 6 wk: Admit with early invasive strategies

The patient’s HEART score in this question would be 2 (1 point for age and 1 point for hypertension as a risk factor). This categorizes the patient as low risk for a MACE over the next six weeks. The appropriate course of action for this patient would be discharge home with prompt outpatient follow-up (Choice B). Admission for cardiac testing (Choice D) would be warranted for a moderate-high risk HEART score. Prescribing a benzodiazepine (Choice C) would not be warranted as this patient is asymptomatic and the pain episode is vague and atypical. Benzodiazepines are sometimes useful in patients with chest pain due to anxiety. Cardiology consultation (Choice A) would not be warranted as the patient has a low HEART score, is currently asymptomatic with normal imaging, blood work and troponin, and a normal EKG. Correct Answer: B 

References

Smith LM, Mahler SA. Chest Pain. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill; Accessed August 17, 2020. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=219641169

Wieters J, McDonough J, Catral J. Chest Pain. In: Stone C, Humphries RL. eds. CURRENT Diagnosis & Treatment: Emergency Medicine, 8e. McGraw-Hill; Accessed August 17, 2020. https://accessmedicine.mhmedical.com/content.aspx?bookid=2172&sectionid=165059275

[cite]

Drop the Beat! – Adenosine in SVT

Drop the Beat! – Adenosine in SVT
~ Mohammad Anzal Rehman, UAE ~ Leave a comment

Supraventricular tachycardia (SVT) is defined as a dysrhythmia that originates proximal to (or ‘above’) the atrioventricular (AV) node of the heart. It commonly manifests as a regular, narrow complex (QRS interval < 120ms) tachycardia in affected patients. It is most frequently attributable to re-entrant electrical conduction through accessory pathways in the heart, with typical Electrocardiogram (ECG) findings depicting ventricular rates of 150 to 250 beats/min without the preceding P wave usually seen in sinus tachycardias. [1,2]

In the stable adult patient presenting with SVT, where no ‘red flags’ such as shock, altered mental state, ischemic chest pain or hypotension are present, management typically begins with an attempt to convert the rhythm back to its baseline sinus state using vagal manoeuvres.[3] Vagal manoeuvres such as the carotid sinus massage and the Valsalva manoeuvre are effective first-line therapies, terminating approximately 25% of spontaneous SVTs,[4] with the newer, modified Valsalva manoeuvre showing even greater efficacy of 43% conversion.[5] When these fail or are otherwise not feasible to use in patients, management involves the administration of a drug called Adenosine.

The Evolution of Adenosine Use for SVT

In 1927, studies found that the injection of extracts from cardiac tissue into animals appeared to decrease heart rates and that this effect was attributable to an ‘adenine compound’.[6] This compound was later identified as Adenosine, comprised of the purine-based nucleobase Adenine attached to a ribose sugar. Fifty years after its initial discovery, Adenosine began to emerge as a treatment for stabilizing SVTs and has remained a mainstay in its management ever since.[7]

Current guidelines recommend Adenosine for the management of SVT, usually administered through a peripheral intravenous (IV) access initially as a 6 mg bolus. Adenosine has an extremely short half-life (less than 10 seconds) and is therefore rapidly metabolized soon after it enters the body.[8] Therefore, IV dosage is commonly followed by a 20 mL rapid saline flush to facilitate the drug’s transport to cardiac tissue where it can act before being broken down into inactive metabolites. If the 6mg dose does not convert the SVT back to sinus rhythm, subsequent doses are given at 12 mg, also followed by 20-mL saline for rapid infusion.

Pro-Tip: Single syringe technique

Before we dive into the concept of the single syringe method of administering Adenosine, take a look at the segment above. How would you give 6 mg of Adenosine through an IV site, making sure a total of 20 mL saline follows right after, in enough time to make sure you don’t waste that precious 10-second half-life of Adenosine? In many places, one of the two methods are used to make this happen:

  1. Use an IV line to push Adenosine > remove syringe > push 10 mL saline using a pre-filled syringe > remove syringe > push 10mL saline using a second pre-filled syringe.
  2. Fancier places use what’s known as a stopcock, a device usually with 3 ports attached to the IV site. Adenosine syringe is attached to one port and a 10 mL saline flush is attached at a separate port. The process looks something like this: Push adenosine through stopcock port > turn stopcock to open saline port’s access to IV site > push 10 mL saline flush > push an additional 10 mL saline using second syringe or remainder of a 20 mL prefilled syringe.

Now we all know that nurses are indistinguishable from ninjas at times when handling IV medication. However, even the most experienced practitioner is not immune to the occasional stumble when switching between the various syringes and swivels required in the methods above. In fact, a study in 2018 found that, in pediatric patients, adenosine given using the stopcock method delivered suboptimal doses.[9]

In an attempt to improve administration time, a potential work-around was proposed where adenosine could be combined with the flush solution in one 20 mL syringe and pushed altogether.[10] This potentially eliminates any time wasted changing syringes and manipulating stopcocks, but does it still work the same? Fortunately, a few studies have demonstrated the feasibility of the single syringe method, with non-inferior efficacy compared to standard methods of drug administration.[11,12]

Caveats: Coffee Conundrums

Let’s talk a bit about dosage. We mentioned above that guidelines recommend starting at 6 mg and moving to 12 mg for subsequent dosages. These dosages assume uninhibited action of adenosine at its receptors which, unfortunately, may not always be the case in patients. What would inhibit adenosine’s activity, I hear you ask? You’ll want to put down that Caramel Macchiato because the answer (pause for dramatic effect) … is coffee – caffeine to be exact.

Caffeine is known to work by antagonizing adenosine receptors, thereby decreasing adenosine’s biologic effect.[13] A component in many frequently consumed beverages, such as coffee, tea, energy drinks and sodas, and with a half-life of approximately 4-5 hours, caffeine is very likely to be present in the bloodstreams of many Emergency Department patients (and doctors). A 2010 multi-centre study in Australia found that recent ingestion of caffeine less than 4 hours prior to a 6 mg adenosine bolus significantly reduced its effectiveness in treating SVT. [14]

This makes it all the more important to not only include information on any known recent beverage consumption during history taking for patients presenting with SVT, but also to potentially increase dosage for patients with a confirmed or suspected recent ingestion of caffeine. In such cases, it would be reasonable to start at 12 mg adenosine as the first dose, followed by 18 mg subsequent dosages to manage SVT.[15]

A 2010 multi-centre study in Australia found that recent ingestion of caffeine less than 4 hours prior to a 6 mg adenosine bolus significantly reduced its effectiveness in treating SVT.

A. Rehman Tweet

References and Further Reading

  1. Bibas, L., Levi, M., & Essebag, V. (2016). Diagnosis and management of supraventricular tachycardias. CMAJ : Canadian Medical Association journal = journal de l’Association medicale canadienne, 188(17-18), E466–E473. https://doi.org/10.1503/cmaj.160079
  2. Mahtani, A. U., & Nair, D. G. (2019). Supraventricular Tachycardia. The Medical clinics of North America, 103(5), 863–879. https://doi.org/10.1016/j.mcna.2019.05.007
  3. Advanced Cardiac Life Support Provider Manual, American Heart Association, Mesquite 2016
  4. Lim, S. H., Anantharaman, V., Teo, W. S., Goh, P. P., & Tan, A. (1998). Comparison of Treatment of Supraventricular Tachycardia by Valsalva Maneuver and Carotid Sinus Massage. Annals of emergency medicine, 31(1), 30–35.
  5. Appelboam, A., Reuben, A., Mann, C., Gagg, J., Ewings, P., Barton, A., Lobban, T., Dayer, M., Vickery, J., Benger, J., & REVERT trial collaborators (2015). Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised controlled trial. Lancet (London, England), 386(10005), 1747–1753. https://doi.org/10.1016/S0140-6736(15)61485-4
  6. Drury, A. N., & Szent-Györgyi, A. (1929). The physiological activity of adenine compounds with especial reference to their action upon the mammalian heart. The Journal of physiology, 68(3), 213–237. https://doi.org/10.1113/jphysiol.1929.sp002608
  7. Delacrétaz E. (2006). Clinical practice. Supraventricular tachycardia. The New England journal of medicine, 354(10), 1039–1051. https://doi.org/10.1056/NEJMcp051145
  8. Kazemzadeh-Narbat, M., Annabi, N., Tamayol, A., Oklu, R., Ghanem, A., & Khademhosseini, A. (2015). Adenosine-associated delivery systems. Journal of drug targeting, 23(7-8), 580–596. https://doi.org/10.3109/1061186X.2015.1058803
  9. Weberding, N. T., Saladino, R. A., Minnigh, M. B., Oberly, P. J., Tudorascu, D. L., Poloyac, S. M., & Manole, M. D. (2018). Adenosine Administration With a Stopcock Technique Delivers Lower-Than-Intended Drug Doses. Annals of emergency medicine, 71(2), 220–224. https://doi.org/10.1016/j.annemergmed.2017.09.002
  10. Hayes, B.D. (2019). ‘Trick of the Trade: Combine Adenosine with the Flush’. Academic Life in Emergency Medicine Blog Post https://www.aliem.com/trick-of-trade-combine-adenosine-single-syringe/
  11. Choi, S.C., Yoon, S.K., Kim, G.W., Hur, J.M., Baek, K.W., & Jung, Y.S. (2003). A Convenient Method of Adenosine Administration for Paroxysmal Supraventricular Tachycardia. Journal of the Korean society of emergency medicine, 14, 224-227.
  12. McDowell, M., Mokszycki, R., Greenberg, A., Hormese, M., Lomotan, N., & Lyons, N. (2020). Single-syringe Administration of Diluted Adenosine. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine, 27(1), 61–63. https://doi.org/10.1111/acem.13879
  13. Ribeiro, J. A., & Sebastião, A. M. (2010). Caffeine and adenosine. Journal of Alzheimer’s disease : JAD, 20 Suppl 1, S3–S15. https://doi.org/10.3233/JAD-2010-1379
  14. Cabalag, M. S., Taylor, D. M., Knott, J. C., Buntine, P., Smit, D., & Meyer, A. (2010). Recent caffeine ingestion reduces adenosine efficacy in the treatment of paroxysmal supraventricular tachycardia. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine, 17(1), 44–49. https://doi.org/10.1111/j.1553-2712.2009.00616.x
  15. Hayes, B.D. (2012). ‘Is the 6-12-12 adenosine approach always correct?’ Academic Life in Emergency Medicine Blog Post https://www.aliem.com/is-6-12-12-adenosine-approach-always/
[cite]

Question Of The Day #12

question of the day
~ Joseph Ciano, USA ~ Leave a comment

Which of the following medications should be avoided to prevent worsening of this patient’s condition?

  • A) Aspirin
  • B) Ibuprofen
  • C) Antacids
  • D) Nitroglycerin

This elderly female patient presents with chest pain described as post-prandial burning, radiating to the shoulders, and with associated nausea and diaphoresis. Burning chest pain after eating supports diagnoses, such as peptic ulcer disease, gastritis, gastroesophageal reflux, or biliary disease. However, chest pain that radiates to both shoulders (2.58 likelihood ratio) or has associated diaphoresis (1.50 likelihood ratio) should be very concerning for acute myocardial infarction (Smith & Mahler, 2020). Associated symptoms that should raise concern for acute coronary syndrome are any radiation of the chest pain, pain worsened with exertion, associated nausea or vomiting, pain described as pressure or squeezing, pain with associated diaphoresis, and pain described as feeling similar to prior ischemic events. This patient’s EKG demonstrates an inferior ST-segment elevation myocardial infarction (STEMI). This is indicated by two or more inferior EKG leads (II, III, and aVF) showing ST-segment elevation greater than 1 mm and reciprocal ischemic changes indicated in lateral leads (I, aVL). Aspirin (Choice A) should be given to all patients with high suspicion for ACS, assuming there are no contraindications. This patient has a confirmed STEMI on her EKG and should receive Aspirin for its antiplatelet effects. Ibuprofen (Choice B) may help the patient’s pain, but likely would not acutely worsen the patient’s clinical condition. Antacids (Choice C) are relatively benign medications, and they would be unlikely to worsen the patient’s clinical condition. Nitroglycerin (Choice D) is often given in patients with anginal chest pain for pain relief. In many inferior STEMIs, nitroglycerin can cause a dangerous drop in blood pressure and should be avoided. These patients may have infarction of the right ventricle, which makes these patients sensitive to nitrates and prone to precipitous drops in blood pressure. IV fluids are the preferred initial therapy in the setting of hypotension. About 40% of patients with an inferior STEMI have concurrent right ventricular infarction. About 80% of inferior STEMIs are caused by occlusions in the right coronary artery (RCA) and about 18% are from an occlusion in the left circumflex artery (LCx). Occluded vessels in both territories can cause right ventricular infarction. Correct Answer: D  

References

Smith LM, Mahler SA. Chest Pain. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill; Accessed August 17, 2020. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=219641169

Burns, E. (2019) Inferior STEMI. Life in the Fast Lane. Accessed August 17, 2020. https://litfl.com/inferior-stemi-ecg-library/

[cite]

Hypokalemic Periodic Paralysis in the ED

Hypokalemic Periodic Paralysis in the ED
~ Sumaiya Hafiz, UAE ~ 1 Comment

Case Presentation

A middle-aged man with a two days history of weakness in his legs. The patient works as a construction worker and is used to conducting heavy physical activity.

After a thorough history and examination, the weakness was reported in the lower extremities with a power of 2/5, whereas the power in upper extremities was 4.5/5, Achilles tendon reflex was reduced, plantar response and other reflexes were intact, with normal sensation. Rest of the examination is unremarkable.

The vitals are within normal ranges, Blood investigations include – Urea and electrolytes, liver and renal function, full blood count, thyroid function tests, creatine kinase, urine myoglobin, vitamin B12 and folic acid levels.

Potassium level was 1.7 mEq/L (normal 3.5-5.5), and all other parameters were within normal ranges.

The ECG showed inverted T waves and the presence of U waves. An Example of an ECG:

ECG-hypokalemia

Hypokalaemia

Hypokalemic periodic paralysis is a rare disorder that may be hereditary as the primary cause, or secondary due to thyroid disease, strenuous physical activity, a carbohydrate-rich meal and toxins. The patients are mostly of Asian origin.

The most common presentation is of symmetrical weakness in lower limbs, with a low potassium level and ECG changes of hypokalemia. The patients may have a history of similar weaknesses which may be several years old. An attack may be triggered by infections, stress, exercise and other stress-related factors.

The word ‘weakness’, can lead to physicians thinking about stroke, neurological deficits and other life-threatening illnesses such as spinal cord injuries associated with high morbidity and mortality which need to be ruled out in the ED.

In this case, history and examination are vital. Weakness in other parts of the body, a thorough neurological examination are important aspects.

Patients are monitored and treated with potassium supplements (oral/Intravenous) until the levels normalize. ECG monitoring is essential, as cardiac function may be affected. 

The patient should be examined to assess the strength and should be referred for further evaluation and to confirm the diagnosis.

The differential diagnosis for weakness in lower limb include :

  1. Spinal cord disease (https://iem-student.org/spine-injuries/)
  2. Guillain barre syndrome
  3. Toxic myositis
  4. Trauma
  5. Neuropathy
  6. Spinal cord tumour

References

[cite]