This blog intends to create an educational platform for Emergency Physicians, sharing EM related basics and updates. Every week, I come up with a new post which can be in the form of written material with references/other FOAMed resources OR a 15-20 minute podcast with a written summary. My goal with this blog is to improve Resident education, Academic EM and Flipping the classroom. To get the maximum benefit from this blog, subscribe by your e-mail.
I have completed bits of my EM training from India. Currently I am boarded with credentials from Christian Medical College, Vellore and also from the prestigious Royal College of Emergency Medicine, UK. I am currently working in London as an A&E doctor, trying to appreciate the differences in the practise and culture of Emergency Medicine across different healthcare systems. I have always been an avid FOAMed supporter because FOAMed played an indispensable role during the days of my initial training. Through this blog, I aspire to disseminate knowledge and stay up to date with the EM literature.
As Emergency Physicians, declaring unexpected bad news is a part and parcel of our job. On one of the most stressful shifts that I have had so far, I remember declaring 3 people dead over a span of 8-10 hours. This can be an extremely challenging task which if not done appropriately can have long standing consequences, not only on the family members of the deceased but also on the physician who breaks the news. Unfortunately, not much attention is paid on how to address this issue in many fields of medicine and only a few specialties receive the right kind of training of doing do such as Emergency Medicine, Critical Care, Palliative Medicine and Oncology. Moreover, even in various life support courses, this particular skill is seldom taught.
Declaring a sudden unexpected death in Emergency Department is quite different from what happens in the Oncology/Palliative Care wards or even in the ICU. In case of a sudden death in the ED, families have a tough time in absorbing the news whereas settings like ICU/Oncology/Palliation wards often provide enough time for the family to adapt the situation.
Here is a framework on how can we do this in the ED: 1. Setting the scene
To begin with, we need to set the stage right, ensuring privacy and giving respect to the family members. Introduce yourself, confirm their identity/relationships and most importantly know the name of the deceased. You have 1-2 minutes to set this right, connect with them, making them feel important and creating a rapport. To accomplish these, look professional, demonstrate empathy, watch you body language, voice tone and expressions. Also turn your phones on silent modes.
I am sorry to meet you in these circumstances. This is going to be a tough conversation for us.
I would also recommend to involve a social worker/nurse right, a chaplain and a medical student or resident with you. They can take control of the situation and provide continued support if you need to leave the room urgently for some reason and for a med student, this is the best opportunity to learn this skill.
This is not like a 1980-90s Bollywood flick, where typically a doctor exits from the operation theatre, shakes his head and says "I am sorry, he is no more" and then walks away. Declaring death is one of the hardest jobs that emergency physicians do and this can be very exhausting if done without apt training.
I believe that the most senior physician present in the ED should take the responsibility of doing this task. The gives a sense of reassurance to the family. A med student or a fresh trainee should never do this alone unless he has been appropriately trained.
2. Breaking the News - Crux of the matter
After a quick introduction, avoid beating around the bush and building unnecessary tension. Come to the point fast and be succinct. You might consider them asking their view point and understanding of the circumstances so far, but avoid asking too many details. Try and deliver the news 2-3 minutes into the encounter. And remember, once you say the work "Death" or "Dead", just stay quiet and let them break the silence. Don't be afraid of silence and allow time for people to imbibe the event. If they break down, give them time and offer tissues or water.
The less you say, the better it is. As physicians, we tend to mention minute details such as:
During resuscitation, we did chest compressions, administered adrenaline and delivered300Jshock but could not bring him back. It seems like he suffered from a refractorycardiac arrhythmia.
Using medical jargon along with providing these minute details might sound a bit defensive and it is best to avoid doing this. It only adds to the confusion. Keep the conversation simple, clear and to the point. If the family witnessed the resuscitation, then they would already know the kind of efforts that you made, which helps them in understanding things better.
3. Continuation of support
At the first place, try to give them uninterrupted time but if there is an emergency and you need to leave, excuse yourself and let the nurse and the social work over take over.
I am going to excuse myself for a while. We have Sister XYZ and our social worker (XYZ) here to help you out further. I will be available in a few minutes to answer any questions that you might have.
Social Workers play a vital role here in terms of helping the family understand about the next steps such as documentation, issuing of a death certificate and preparation of funeral. They can also provide assistance if the relatives want to call and speak to someone.
As a physician, you need to visit them again to ask if they have any questions or concerns or if they would like to see the deceased person or perform some religious rituals. And if they want to see or touch the the dead body, take a few minutes to make the body look presentable and warn them for any disfigurement that they might see.
Follow the local organ donation policies, involve the organ donation co-ordinator for this. I personally think you need not speak about organ donation with the family in a case of sudden unexpected death. This is best left to the organ transplant co-ordinator.
But if your institute has a stringent policy that states emergency docs need to initiate this discussion, then start with something like this:
I am sorry for asking this Mr. XYZ, but have you ever had any discussions about organ donation ?
Does (Name of the deceased) has an organ donation card?
In addition, you also need to mention the need to perform an autopsy if it is a medico-legal case. The brunt of doing this falls on the emergency physicians. The family (regardless of the cause of death) is never in favour of a post-mortem examination. If you think autopsy is required, be assertive on that and consider saying something like this:
Since this is an medically unexplained death/Road Traffic Accident. I am bound to fill a medico-legal form which is then passed on to the police department. Unfortunately, I don't have a say in this and things are going to move as per the law of the land.
Many hospitals also give follow up calls to the families to ask about their well-being 2-3 weeks after the event.
Breaking a bad news might be an everyday thing for you, but for a family, this is possibly the most stressful day in the lives or probably a life changing event. Therefore, we need to keep everything aside and give them uninterrupted attention for a few minutes. They are going to remember what you say for the rest of their lives, so be sensitive and considerate.
MRCEM exams for June 2016 are approaching and the stakes are high. I see candidates fumbling and getting overtly anxious, especially about the part C exam. So I am going to try and help you guys out with part C by doing 1 on 1 tutoring via Skype/ Facetime from 28-31st May 2016. If you do not want to spend on live workshops because of your prior commitments or limited budget then you can enrol for one of these mock exams. The thing with these sessions is that you can avoid spending on travel and accommodation and save a ton of time. My goal is to provide you a meaningful feedback which I believe can transform your results. It is essentially hard to judge yourself if you are practising with your colleagues who are on the same page.
Scheduling and fee:
You can schedule a
Two station mock for 1000 INR (25 minutes: includes station time and a brief verbal feedback) OR
Five station mock for 2500 INR (60 minutes: includes station time and an elaborate verbal and written feedback mentioning the strengths and weaknesses of the candidate)
The focus of these sessions will be to give you an insight about where you stand in your preparation and what you need to work on, during the week prior to the real exam.
I don't want you guys to waste money on this and therefore I suggest that you practise a few stations among your friends and then join a 1-1 session with me to get evaluated. I have extremely limited time and very few spots available on first come first serve basis. You can contact me through whatsapp or e-mail to get further details on payment.
You can drop in your messages and I will revert back to you on 27 May 2016.
I am an Emergency Physician who is interested in teaching and finding out ways on how to advance medical education. I love to teach and meet people who are at different stages of academic ladder. I was trained in EM at Christian Medical College, Vellore and Apollo Hospitals, Hyderabad. I am also certified by Royal College of Emergency Medicine and I have been through MRCEM part A,B,C and passed all the three exams on the first attempt. So I can completely relate with you and understand what you will be going through. Let me know if you have any further questions or concerns.
TakoTsubo Cardiomyopathy (TTC), also known as broken-heart syndrome, apical ballooning syndrome or stress-induced cardiomyopathy. It is a reversible cardiomyopathy characterised by transient systolic ventricular dysfunction with a clinical presentation indistinguishable from acute myocardial infarction but in the absence of significant coronary artery obstruction. This condition is frequently precipitated by sudden, stressful emotional events, occasionally due to physiologic stress such as sepsis, non-cardiac surgery, and subarachnoid hemorrhage.
The term "Takotsubo" was coined to describe the unusual shape of the left ventricular during systole.Typically, the mid to apical segments of the left ventricle are akinetic and the spared, basal walls exhibit compensatory hypercontractility. Takotsubo is a pot with round base and narrow neck used in Japan for trapping octopuses and has a similar appearance to this apical ballooning.
TTC occurs most commonly in postmenopausal women and has a very good prognosis. Acutely, patients are often critically ill with heart failure, arrhythmias, shock, LVOT obstruction, thromboembolism but symptoms resolve quickly and death is rare.
The pathophysiologic basis of TTC has not been conclusively determined but several mechanisms have been proposed. The underlying histopathological findings on myocardial biopsy are distinctly different from those of coagulation necrosis seen in typical atherosclerotic epicardial artery occlusion and myocardial infarction.
Catecholamine overload and myocardial stunning
Multi-vessel coronary artery spasm with resultant ischemia and stunned myocardium
Spontaneously aborted myocardial infarction
Microvascular dysfunction and myocarditis
TTC has been reported to account for 1-3% of all acute coronary cases.About 90% of cases reported are in post-menopausal women ages 58-75 years old. The clinical presentation of TTC is often identical to acute myocardial infarction (AMI). Most patients with takotsubo cardiomyopathy present with typical anginal chest pain, dyspnea, ischemic changes on electrocardiogram (ECG), and elevated cardiac markers.Emotional stress, such as news of the death of a family member, divorce, or public speaking, is implicated as the trigger in approximately two-thirds of patients.
ECG changes and cardiac biomarkers
The most common abnormality on the ECG is ST elevation and T-wave inversion in the precordial leads. However, there may be some population differences in presenting signs and specific ECG changes should be considered suggestive but not diagnostic of TTC. Modest elevation of cardiac biomarkers is often observed in TTC.
Due to the dramatic clinical presentation and high suspicion for acute myocardial infarction, most patients undergo emergent coronary angiography. Typical findings in TTC are normal epicardial coronaries, mild non-obstructive atherosclerosis, or rarely coexistent coronary artery disease.Therefore, TTC is a diagnosis of exclusion which can only be made after coronary angiography.It should be on the differential diagnosis in any post-menopausal women over 50 years old presenting with chest pain and ischemic ECG changes particularly in the setting of emotional stress. Furthermore it should also be considered in critically ill patients with sudden hemodynamic compromise and/or heart failure.
Mayo Clinic proposed diagnostic criteria in 2004 for TTC which includes four components:
(1) Transient hypokinesis, akinesis, or dyskinesis of the left ventricular mid seg- ments with or without apical involvement; the regional wall motion abnormalities extend beyond a single epicardial vascular distribution; a stressful trigger is often, but not always present
(2) Absence of obstructive CAD or angiographic evidence of acute plaque rupture
(3) New electrocardiographic abnormalities (either ST-segment elevation and/or T wave inversion) or modest elevation in cardiac troponin
(4) Absence of pheochromocytoma and myocarditis
Ventriculography reveals apical ballooning, with characteristic sparing of the basal segments and akinesis of the mid and apical left ventricle. However, variants of this pattern have been described.In patients with typical TTC, the wall motion abnormality usually extends beyond the distribution of a single coronary artery.
Echocardiography can detect and measure the degree of left ventricular outflow (LVOT) obstruction and associated systolic motion of the anterior mitral valve and significant mitral regurgitation.
LVOT obstruction is reported to occur in 25% patientsand can have a major impact on acute management. In patients with hemodynamic compromise and shock, inotropes would worsen this situation and betablockers and pure vasopressor pharmacologic or mechanical support may be needed. The typical findings on cardiac MRI include the absence of delayed gadolinium hyperenhancement. This is specific to TTC and can help differentiate it from myocarditis and acute myocardial infarction in which delayed hyperenhancement is present.
Takotsubo cardiomyopathy has an excellent prognosis, with full and early recovery in virtually all patients. The majority of patients have normalization of LVEF within a week and all patients by 4-8 weeks. Long-term survival is similar to the general population.
The goals of treatment are usually conservative, supportive care. The therapy is guided by the patient’s clinical presentation and hemodynamic status. Despite the possible causal role of catecholamines in the disorder, patients who present in cardiogenic shock, and in the absence of LVOT obstruction, may be treated with inotropes.
Alternatively patients may derive further benefit from IABP and VADs.
If LVOT obstruction is present with cardiogenic shock, inotropes should be avoided and phenylphrine is the pressor agent of choice often combined with betablockade.
Anticoagulation is reserved for those with ventricular thrombus or evidence of embolic events.
Takotsubo cardiomyopathy is an acquired cardiomyopathy which is a differential diagnosis of acute coronary syndrome.
It is characterized by transient systolic ventricular dysfunction with regional wall motion abnormalities beyond a single vascular territory in the absence of significant epicardial coronary artery obstruction.
Acute emotional/ physical stressor immediately preceding the acute coronary syndrome is a common presentation. Catecholamine excess and cardiotoxicity is the most likely underlying mechanisms.
Supportive treatment is the mainstay of therapy.
Kurisu S, Kihara Y. Clinical management of takotsubo cardiomyopathy. Circ J. 2014. 78 (7):1559-66.
Prasad A, Lerman A, Rihal CS. Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction. Am Heart J. 2008 Mar. 155(3):408-17.
Bybee KA, Kara T, Prasad A, et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med. 2004 Dec 7. 141(11):858-65.
Merchant EE, Johnson SW, Nguyen P, Kang C, Mallon WK. Takotsubo cardiomyopathy: a case series and review of the literature.WestJEM. 2008. 9:104-11.
Brugada Syndrome was first described by Pedro and Josep Brugada in 1992 in eight otherwise healthy patients with sudden and aborted cardiac death, in whom they found “right bundle branch block and persistent ST segment elevation in leads V1 to V3”. It’s incidence seems to be particularly high in Southeast Asia where it had been previously described as Sudden Unexplained Nocturnal Death Syndrome (SUNDS), The condition is also believed to be one of the potential causes of sudden infant death syndrome and sudden cardiac death in young children.
The condition is supposed to be due to a cardiac sodium channel mutation. ECG changes can be transient with Brugada syndrome and can also be unmasked or augmented by severe, schema and medications.
Check out this short video on Brugada Syndrome, by the legendary "Amal Mattu"
Different patterns of STE in Brugada Syndrome:
1) Coved: a coved-type (straight or convex upward) terminating in an inverted T-wave, more predictive of arrhythmic events.
2) Saddle: Concave upward
Diagnostic Criteria: This ECG abnormality must be associated with one of the following clinical criteriato make the diagnosis:
Documented ventricular fibrillation or polymorphic ventricular tachycardia
Family history of sudden cardiac death at <45 years old
Coved-type ECGs in family members
Inducibility of VT with programmed electrical stimulation
Nocturnal agonal respiration
Definite Treatment Pharmacological treatment does not protect against recurrent events and implantation of an cardiac defibrillators is the only proven effective treatment in preventing sudden death in patients with the Brugada syndrome.
The term “Brugada Syndrome” is used when the Brugada ECG is
accompanied by symptoms of syncope or cardiac arrest.
Knowledge of Brugada ECG pattern is paramount for Emergency Physicians.
Patients with suspected Brugada Syndrome require an early cardiology or electrophysiology opinion.
Definite treatment is implantation of a defibrillator to prevent death from sudden ventricular arrhythmia.