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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. 

Monday, August 21, 2017

Vertigo, “Answers” by EM Lyceum


  1. What elements of history do you find most reliable in differentiating central from peripheral vertigo?
Dizziness is the cause of over 10 million ambulatory care visits per year, 25% of which are seen in emergency departments around the US (Newmann-Toker, 2008).  Vertigo is a subset of dizziness in which patients have a false sense of spinning or movement in either themselves or their environment.  The causes of vertigo are numerous, yet are most often categorized as being either of peripheral or central etiology.  Peripheral etiologies include benign diagnoses such as benign paroxysmal positional vertigo (BPPV), vestibular neuritis/labrynthitis, Meniere’s disease, as well as more serious diagnoses such as herpes zoster oticus, and aminoglycoside toxicity.  Central etiologies, however, often include more dangerous pathologies such as brainstem ischemia, cerebellar infarction/hemorrhage, and vertebral artery dissection. Central causes may also include slightly less emergent diagnoses such as migrainous vertigo, multiple sclerosis and Chiari malformations.   The challenge for the ED physician has always been to differentiate the dangerous central causes from the benign peripheral etiologies using history and physical exam, as diseases in both categories often present with vertigo as a major symptom.
On history, the most amount of helpful information can be gleaned from teasing out the timing/duration of the vertiginous episodes.  Although this information may not differentiate central versus peripheral, as lots of overlap exists, it can help narrow the differential diagnosis.  In patients presenting with an acute, prolongedepisode of severe vertigo (i.e., acute vestibular syndrome) the two primary pathologies to consider are vestibular neuritis and cerebellar stroke.  In patients with recurrent, positional vertigo one should consider BPPV as well as Chiari malformation, cerebellar tumors, and multiple sclerosis.  In patients with recurrent, non-positional vertigo,  Meniere’s disease and posterior circulation TIA belong on the differential.
It is a misconception that vertigo that is worsened by head/body movement (including Dix-Hallpike maneuver) is the result of a peripheral cause such as BPPV.  However, the exacerbation of symptoms with head movements have been reported in all causes of vertigo (Kubo, 1988).  Others experts argue that patients with dizziness from ANY cause will feel worse with certain position changes (Kerber, 2009).  Therefore, the characteristic that distinguishes BPPV is not simply an exacerbation of vertigo by head movement, but rather, vertigo that is triggered by positional changes, lasts less than one minute, and then returns to normal between attacks (Kerber, 2009).
Another piece of helpful history is the presence of otic symptoms (hearing loss, tinnitus, ear fullness, etc.), which strongly suggests peripheral etiology (Newmann-Toker, 2007).  Some newer evidence, however, does demonstrate that infarctions of the posterior circulation in the distribution of the anterior inferior cerebellar artery (the blood supply to the inner ear), may rarely cause similar otic symptoms (Lee, 2009).
Other pieces of history that may be helpful include a recent hyper-extension injury ortrauma associated with neck pain and vertigo, which may be indicative of a vertebral artery dissection.  Other central nervous system symptoms including diplopia, dysarthria, weakness, truncal ataxia, and sensory loss are often indicative of a central cause.  Patients with significant stroke risk factors (i.e., hypertension, diabetes, atrial fibrillation, smoking, history of vascular disease) may have vertebrobasilar insufficiency as the cause of their vertigo (Kerber, 2006).  Medications such as aminoglycosides may cause peripheral vertigo, whereas phenytoin can result in cerebellar toxicity and associated vertigo.
Components of the history that may not be as helpful include the presence of nausea or vomiting, which can be seen in both peripheral and central vertigo (Baloh, 1998).  There is also no evidence supporting the presence of a concurrent viral syndrome to be indicative of a peripheral ethology.

2.     What elements of physical exam do you find most reliable in differentiating central from peripheral vertigo?
The crux of being able to distinguish central from peripheral vertigo lies largely in the physical examination.  Hard focal neurological signs (i.e., hemiplegia, hemisensory loss, ataxia, dysarthria, ophthalmoplegia, etc.) clearly point to a central etiology, but unfortunately are found in only approximately 50% of patients with posterior strokes (Kattah, 2009).  So how does one go about differentiating between the two types of etiologies in patients who have no hard neurological signs?  As they say, the truth lies in the eyes…
The classic teaching about nystagmus stills holds up quite well as an accurate method of distinguishing central from peripheral vertigo (Baloh, 2003).  Nystagmus of peripheraletiology is generally found to be horizontal in nature and unidirectional (the fast component of the nystagmus always beats in the same direction, regardless of which way you extend the patient’s gaze).  On the contrary, nystagmus of central etiology is often purely torsional or vertical in nature (usually down-beating nystagmus) and is bidirectional (the fast component of the nystagmus changes directions depending on which direction you extend the patient’s gaze).
              Nystagmus, peripheral                                     Nystagmus, central
Type                Horizontal                                                       Pure torsional or vertical
Direction       Unidirectional                                                 Bi-directional
Although these are reliable physical examination tests, a group of researchers at Johns Hopkins University have developed an even simpler and more accurate 3-step bedside ocular physical examination. They posit that it can quickly and accurately differentiate acute vestibular neuritis from a posterior stroke in patients with continuous vertigo (Kattah, 2009).  The series of tests is called the HINTS exam and is comprised of 3 components: Head Impulse testing, bi-directional Nystagmus, and Test of Skew.  In their prospective, cross-sectional study, they performed the HINTS exam at the bedside of 101 patients in an academic hospital stroke center to try and differentiate between those patients with central versus peripheral etiologies of their vertigo.  Later they confirmed their diagnoses using MRI with diffusion-weighted imaging.  They concluded that the presence of either a normal horizontal head impulse test, direction-changing nystagmus in eccentric gaze, OR skew deviation was 100% sensitive and 96% specific for stroke.  With  MRI having a 12% false negative rate within the first 48 hrs of symptom onset, the HINTS exam was purported by this group to be more sensitive than MRI in initial diagnosis of posterior circulation strokes (Kattah, 2009).
For a video demonstrating how to do the HINTS exam please visit the site of Dr. David Newmann-Toker at: http://novel.utah.edu/Newman-Toker/collection.php#

3.     When do you obtain imaging in a patient with vertigo?  Which study do you use and why?
Brain imaging should be obtained in patients when there is concern for a central cause of  vertigo such as a posterior circulation stroke or vertebrobasilar insufficiency.  A non-contrast head CT (NCHCT) is often the first diagnostic study ordered because of its accessibility in most emergency departments.  NCHCT, however, has poor diagnostic utility in diagnosing lesions of the posterior fossa, because of the amount of bone artifact present.  NCHCT has a sensitivity of only about 16% in the diagnosis of acute ischemic posterior stroke (Chalela, 2007).  As a result, NCHCT should never be used to rule out the diagnosis of stroke in a patient with a possible central etiology.  The only situation where NCHCT reliably identifies a central cause of vertigo is in hemorrhagic infarctions of the cerebellum, in which acute blood is usually evident immediately by CT.  Unfortunately, these account for only 4% of central causes of acute vestibular syndrome.
Instead, the test of choice when a central cause of vertigo is suspected is an MRI, as it allows a better view of the posterior fossa.  In contrast to CT, MRI has a sensitivity of about 80% in detecting lesions of the posterior fossa within 24 hours of symptom onset (Tarnutzer, 2011).  The obvious disadvantage of MRI is it’s often not readily available in the emergency department within a short period of time.  If the integrity of the posterior circulation needs to be assessed, an MRA may also be useful in detecting vertebrobasilar stenosis or dissection.  Although MRI is clearly more sensitive than CT in detecting posterior strokes, MRI was found to have a false negative rate of about 12% in the original HINTS study, meaning that it fared worse than the bedside HINTS exam in detecting posterior strokes (Kattah, 2009).


4.     In which, if any, patients do you perform a Dix-Hallpike maneuver?  In which patients do you perform an Epley maneuver? 
The Dix-Hallpike maneuver is done to confirm the diagnosis of BPPV in patients with recurrent, positional vertigo.  It tests for the presence of an otolith in the posterior semi-circular canal (the most common cause of BPPV).   It is important to understand that while doing the Dix-Hallpike maneuver, vertigo may be reproduced in patients with both central and peripheral etiologies.  Therefore, the most important aspect of the test is  evaluation of the nystagmus, not the reproducibility of the vertigo.  In a patient with BPPV, the Dix-Hallpike maneuver should elicit nystagmus after a latency of a few seconds, and the nystagmus should last about 15-25 seconds only (Kerber, 2009).  Any nystagmus that persists longer than this should not be considered to be a result of BPPV, and other possible central causes should be considered.  The Dix-Hallpike maneuver has a sensitivity of about 50-88% in patients with BPPV (Hoffman, 1999).
For a video on how to properly perform the Dix-Hallpike maneuver, visit the website of Dr. David Newman-Toker: http://novel.utah.edu/Newman-Toker/collection.php#
When a patient with suspected BPPV has a positive Dix-Hallpike maneuver, the patient can be taken directly into the Epley maneuver in an attempt to reposition the otolith and treat the BPPV.  The efficacy of the maneuver can be tested by rechecking the Dix-Hallpike test after the Epley maneuver is performed. The nystagmus should no longer be present if the Epley maneuver was successful.  If the Dix-Hallpike test shows continued nystagmus, the Epley maneuver can be repeated.
Von Brevern, et al. demonstrated that, when compared to a sham maneuver, the Epley maneuver was successful in 80% of patients (compared to 10% of patients in the sham group) in relieving symptoms of vertigo and nystagmus at 24 hours after treatment (von Brevern, 2006).  Further studies have also outlined the success of the Epley maneuver, compared to sham maneuvers, as a useful method of acute treatment as well as long-term treatment.
 5.    Bonus question:  Which medications do you use to treat vertigo? 
In the treatment of acute vertigo, medications should be given to treat nausea/vomiting as well as the acute episodes of vertigo.  Nausea and vomiting can be treated  in the emergency department with any number of phenothiazine anti-emetics including ondansetron, metoclopramide, or promethazine, to name a few.  These medications may also acutely decrease the symptoms of vertigo experienced by a patient.  IV fluids should also be given to assist in the repletion of volume lost through multiple vomiting episodes.
In order to acutely and effectively treat the symptoms of vertigo, often caused by abnormalities in the vestibular system, vestibular suppressants may be used.  The two major classes of drugs used for this purpose are antihistamines (i.e., diphenhydramine, meclizine, dimenhydrinate, etc.) and benzodiazepines (i.e., diazepam, clonazepam, etc.).  Both classes of medications are complicated by side-effects of drowsiness, which may not be desirable, especially in elderly patients (often worsening their complaints of “dizziness”).  These medications, useful in the initial days of significant vertigo, should be discouraged in daily use after the first 24-48 hours. They are believed to compromise the brain’s ability to compensate for long-term vestibular dysfunction and may delay recovery (Baloh, 2003).
Of the two classes of drugs, antihistamines are often considered to be first-line therapy for vertigo, as they appear to be less sedating than their benzodiazepine counterparts.  In terms of comparative efficacy in alleviating vertiginous symptoms, very little data exists.  One double-blind randomized study by Marill, et al., looked at 74 patients and compared 2mg IV lorazepam to 50mg IV dimenhydrinate in the symptomatic treatment of vertigo in the emergency department. They demonstrated that patients given dimenhydrinate had an increased ability to ambulate, less drowsiness, and were significantly more likely to be “ready to go home” compared with the lorazepam group at the 2 hour mark after treatment (Marill, 2000).

Monday, August 14, 2017

Overtesting and Misinterpretation - Urine Dip Pearls

Interpreting lab tests requires a considerable amount of knowledge and experience. One such test is urine dipstick which is often done in the ED to look for blood, evidence of infection, ketones etc. Since Emergency Departments across the globe are working under tremendous amount of time constraints, tests are now being done based of chief complaints (abdomen pain panel, pleuritic CP panel, Headache panel etc.) instead of clinical suspicion of a diagnosis. While this reduces the time to reach a conclusion, it makes evaluation and medical decision making very complex for a clinician. 

What are we supposed to do with a result that we never expected and we never wanted that to be sent at the first place? Positive hstroponin in a very low risk patient, positive d-dimer in a 16 year old who was hyperventilating or a positive urine dip for nitrites in an asymptomatic patient.





We know that we are overdiagnosing and over-treating UTIs. Rates of Misdiagnosis of UTI are up to 40%. Therefore, it is imperative to have have a pre-test probability before we order a urine dip or microscopy. And if it is already reported before you have actually seen the patient, be comfortable in disregarding the results if it does fit in the clinical scenario. 

Having a clinical questions can help. Ask yourself these two questions before you order any test (not just Urine Dip):

1.What are you looking for in the test. Is it Nitrites or blood or ketones? 
2. What is going to be your next step if the result is positive or negative?



Putting Urine Dip into a clinical context differentiates a clinician from other healthcare providers. Treating positive urine nitrites for UTI - Anyone can do that! 
But Medicine is not that simple!


Key points while interpreting a urine dip:

1. Bacteriuria does not equal UTI
If you send a culture on asymptomatic bacteriuria, you might get a positive culture but what if your patient never had any symptoms? The answer is - do not bother sending urine for testing in asymptomatic patients and do not treat asymptomatic bacteriuria (exceptions - Rx in pregnancy in those who are undergoing a urologic procedure). UTI is a clinical diagnosis, not a lab diagnosis. Colony counts and cultures are pointless without symptoms or clinical suspicion. 

2. Leucocyte Esterase (LE) is indicative of pyuria not UTI
Here is a list of things than can cause pyuria:
  • HIV
  • STDs
  • Appendicitis
  • Urolithiasis
  • Malignancy
  • Nephritis 
  • Dehydration
  • Diverticulitis
  • Indwelling catheters
Once again, results for LE needs to interpreted with a clinical context. In neutropenic patients, urine WBCs may be artificially low despite an infection

3. Nitrites 
Nitrates in the urine are converted to nitrites in the presence of Gram-negative bacteria such as E.coli. A positive nitrite test is a indirect marker of bacteriuria, not always a marker of infection (unless patient is symptomatic).

Nitrites are not produced by S. saprophyticus, Pseudomonas or enterococci, so a negative nitrites does NOT rule out UTI. Also watch your method of sample collection. Almost universally, urine is collected in a non-sterile fashion and thus interpretation should be always in the clinical context. Presence of Epithelial cells indicate a contaminated sample. 


Negative leukocyte esterase and nitrite negative almost rules out UTI


4. Elderly with Altered Mental State and UTI - Not always!
UTI is this scenario is pretty much a diagnosis of exclusion (Rule out Neuro and GI causes before labelling as UTI). Asymptomatic bacteriuria is extremely common in elderly. Rx them based on the history of symptoms and confirm your diagnose with a catheterised sample. When history is compromised due to cognitive issues - Look for fever, chills, elevated WCC, CRP, previous episodes of UTI to gauge your suspicion. If the look stable (normotensive, not tachycardia, no fever) then it is reasonable to hold Abx and convey this to the in-patient teams. 

5. He smells of urine, so we think it is a UTI
Anyone who is unkempt, not looked after well and urinates in his pants is going to smell bad. Bad smell is not always an indicator of Urine Infection. Do not prematurely close the diagnosis here. Smell can be affected by a number of factors such a your hydration status, concentration of urea, diet. Do a complete history and physical and then come to a conclusion. 



Take Home
  • Do not treat asymptomatic bacteriuria
  • Hold Abx if they look stable. Liaise with in-patient teams. 
  • Negative leukocyte esterase and nitrite negative makes UTI highly unlikely

References:

Schulz L, Hoffman RJ, Pothof J, et al. Top ten myths regarding the diagnosis and treatment of urinary tract infections. J Emerg Med. 2016 Jul; 51(1): 25-30. 


Posted by:




              
     Lakshay Chanana
     
     Speciality Doctor
     Northwick Park Hospital
     Department of Emergency Medicine
     England

     @EMDidactic


Monday, August 7, 2017

Ulcerative Colitis - ED Management

Ulcerative colitis (UC) is a chronic inflammatory relapsing and remitting disease of the colon. The etiology is believed to be autoimmune with some genetic component. Peak incidence occurs in the second and third decades of life with characteristic symptom of bloody diarrhoea. The rectum is almost always involved in UC. 

Factors associated with an unfavourable prognosis include higher severity and extent of disease, a short interval between attacks, systemic symptoms, and onset of the disease after 60 years of age.


Clinical Presentation

Crampy abdominal pain, bloody diarrhea, and tenesmus are typical symptoms of UC. The disease is classified as mild, moderate, or severe depending on the clinical manifestations. 

Truelove and Witts criteria


Extra intestinal Manifestations 



Diagnosis

ED diagnosis of ulcerative colitis rests on the following: 
History of abdominal cramps and diarrhea, mucoid stools, stool examination negative for ova and parasites, stool cultures negative for enteric pathogens, and confirmation of diagnosis by colonoscopy.




Treatment


Mild to Moderate attacks
Most of these patients can be treated as outpatients. A combination of oral (2.4 grams/day) and topical mesalamine is used. Topical glucocorticoid enemas or Mesalazine enemas or suppositories (500 milligrams twice a day) are quite effective in distal proctosigmoiditis and have lower systemic side-effect profiles.

If topical therapy is unsuccessful, steroids (40-60md Prednisolone/day) are effective in inducing a remission in the majority of cases. Antidiarrheal agents are generally ineffective and may precipitate toxic megacolon.


Rx of UC based on severity of disease

Severe ulcerative colitis - Treat with IV steroids, fluids, correct electrolyte abnormalities, broad-spectrum antibiotics, melamine. IV cyclosporine (2-4 milligrams/kg per day) or infliximab (5 milligrams/kg) can be effective in fulminant colitis nonresponsive to IV steroids.



Complications
  • LGI Bleed (Most Common)
  • Toxic Megacolon The most feared complication of ulcerative colitis is the development of toxic megacolon. TM occurs as a result of extension of the inflammation beyond the submucosa, causing loss of contractility and dilated colon. Dilation of the colon is associated with a worsening of the clinical condition and development of fever and prostration. Patients with Toxic Megacolon appear toxic with distended, tender and tympanic abdomen. They typically present with fever, tachycardia and shock.

Plain radiography of the abdomen demonstrates a long, continuous segment of air-filled colon greater than 6 cm in diameter. Loss of colonic haustra represent bowel wall edema. Occasionally, features of toxic megacolon, such as leukocytosis, anaemia, dyselectrolytemia, hypoalbuminemia and peritonitis, can be masked in the patient taking corticosteroids.  


Antidiarrheal agents, hypokalemia, narcotics, cathartics, pregnancy, enemas, and recent colonoscopy have been implicated as precipitating factors in toxic megacolon. Rx with nasogastric suction, IV steroids, broad-spectrum antibiotics active against coliforms and anaerobes, and IV fluids. Get a surgical consultation ASAP.
  • Perforation
  • Bowel Obstruction (due to strictures)
  • Carcinoma Colon  (Advanced and prolonged disease)
  • Perirectal fistulas and abscesses 

Disposition
Fulminant attacks of ulcerative colitis need hospitalization for fluid and electrolyte management and careful observation for the development of complications. Patients with complications such as GI Bleed, toxic megacolon, and bowel perforation should also be admitted. In addition to toxic megacolon, the indications for surgery include colonic perforation, massive lower gastrointestinal bleeding, suspicion of colon cancer, and disease that is refractory to medical therapy (large doses of steroids required to control the disease). 

Patients with mild to moderate disease can be discharged from the ED.  It is crucial to arrange close follow-up with gastroenterologist, and any adjustment in medical therapy should be discussed prior to discharge.


References:
  1. https://clinicalgate.com/toxic-megacolon/
  2. Oxford Handbook of Clinical Medicine
  3. Tintinalli's textbook of EM - 8th Edition
  4. http://fromnewtoicu.com/blog/2016/12/28/toxic-megacolon-1
Posted by:



              
     Lakshay Chanana
     
     Speciality Doctor
     Northwick Park Hospital
     Department of Emergency Medicine
     England

     @EMDidactic


Monday, July 31, 2017

The nomenclature of EM postgraduate qualifications in India - Simplified

As Emergency Medicine is a new specialty and there has been a lot of buzz around it, if you are a medical graduate in India wanting to take up Emergency medicine you would definitely be perplexed by the myriad of nomenclatures of EM postgraduate qualifications. As an MBBS pass out when you are vaguely starting to understand what different specialties are and what EM is, just when you think you might have a thing for EM, you probably are bombarded with countless names (of qualifications), each claiming to be superior to one another. Everyone seems to have an opinion about EM (like everything else) - One with a qualification in EM, one without, a doctor who has no idea what emergency medicine is, that homeopath on the crossroad, EVERYONE! Just yesterday when I was walking down the road I even overheard the samosa guy explain to the chaiwala (No no..not Modi!) how one course is better than the other while he unknowingly obstructed an Ambulance passing by with his cart although the ambulance had it's sirens and lights on !!!

So what's this confusion about ? And how does a MBBS student or aspiring EM physician analyze this and make an informed decision and decide what course to join ? Whom to trust when people are claiming everything like popular news channels - "First on EM tv", "You saw it first on nautanki now", "We are the undisputed No.1" and "Exclusive" ?!
So let me just try to dissect each of the popular EM qualifications in India. I will try to list the advantages, drawbacks of each of them. I will try to be as unbiased as possible and try to touch upon some facts pertaining to recent controversies step by step.


1. MD Emergency Medicine:
Like all other MD qualifications, this degree is given by Medical Council of India. Course is run in many medical colleges across India. There are fixed number of seats.
Q: What are the advantages:
- Needless to say it is recognized by MCI as it is run by MCI (kind of dumb point ;-P Filling up the answer sheet will fetch me some extra marks isn't it? Anyway!)
- You can be a faculty in medical colleges and hospitals running DNB after the completion of the course.
- Getting a job after MD shouldn't be a problem at all as MD is a brand in itself irrespective of how good you are.
- Like any other MD final exam, passing is probably not very difficult (well, I don't have a first hand knowledge here but I haven't heard of someone flunking the MD final exams multiple times nevertheless)
- Entry is through NEET. So you definitely have to work hard to earn a seat** (conditions apply)
- You can write MRCEM exam and DNB exam while you are at it! So can be a triple degree holder (if you are a degree fanatic) at the end of your course! (Will explain MRCEM in a bit if you do not know what that is or confused about it)
- On a lighter note you don't have to explain your degree to relatives unlike most other degrees. (Although there's no escaping from explaining what EM is!)

Q: Wow!!! Then is this the perfect, irrefutable, most 'legitimate' EM degrees of all ???
A: Hold on. The answer might not be an absolute no or a blanket yes. There are downsides of course!
- There are many medical colleges where the department of EM is not completely established or to put it in another way there's no concept of emergency medicine. The primary faculty for teaching are not from EM.
Although it can be argued that the origin of EM roots back to surgical specialties and different skills required for an emergency physician can be taught by different specialties, the lack of primary teaching faculty from EM would definitely hamper the 'EM-culture'. While an anesthetist can be a great teacher of airway skills, an orthopod can teach reducing a shoulder like none other, none of them can teach the 'EM-mindset' like an emergency physician, which is the heart of practicing as an emergency medicine doctor.  (Enough, I think I did too much talking there!)
-**Varmaji's beta worked hard, passed MBBS with distinction, studied again, got good rank in NEET, was an adrenaline junkie who wanted to bring a change in people's lives, was interested in EM, got a MD EM seat in a reputed medical college. Passed with flying colors.  Well done. LEGITIMATE!
Sharmaji's beta passed MBBS after Salman threatened him that he will get married before he passes. He once tried to memorize the full form of NEET but then he felt that was completely unnecessary. He thought he would do MD EM because someone said he didn't have to admit patients under him if he did that. He was rich, Sharmaji owned 2 BMWs, he spilled 1.5 crores and BOUGHT a MD EM seat in the same college as Varmaji's beta like you buy a kilo of brinjal (Baingan - I can't kill the Hyderabadi in me) from the market. He also somehow passed. Sharmaji's beta is also MD Emergency Medicine now! LOL! Legitimacy!? LOLOLOL!
--> So, on a serious note, I'm not saying that MD EM is all bad. Neither it's sacred and the BEST just because it is run by MCI. Making blanket statements won't help!
So the bottom-line is - Good score in NEET --> Good college with good EM dept. with preferably faculty from EM --> MD EM --> Good.

2. DNB Emergency Medicine:
Run by NBE (National Board of Examinations) across different hospitals and some medical colleges across India. Like MD, they have fixed number of seats.

Q: What are the advantages:
- Recognized by MCI.
- Can be faculty in medical colleges (There has always been some controversy regarding DNB candidates being asked for some additional experience to work as assistant prof in medical colleges, I'm unsure of the present status) and DNB institutes.
- Entry is via NEET.
- Main factor which might increase the 'LEGITIMACY index' of DNB is that there are no 'management seats'. That means no one can 'buy' DNB seats. You will have to earn them! That's commendable.
- Again getting a job shouldn't be a problem. DNB programs are well known for churning out good doctors historically.
- Final exams are not easy as MD is the general perception. Which is kind of good. When you pass, people know you deserve it.
- You can of course write MRCEM exams while you are at it!

Q: Well, then there are no downsides? That's amazing, isn't it?
A: Nothing is completely blot free! Again some downsides are:
- This one is common: Some hospitals might not have primary faculty from EM.
- Secondary DNB eligibility: Dude, this is a JOKE! Anyone with ANY diploma is eligible for secondary DNB EM. Like Dip microbiology, pathology etc. can take up DNB EM (secondary). What on the earth were they thinking while they made these criteria?! What are they trying to do/achieve ?! Bizarre!
Bottom-line: Good hospital --> DNB EM --> Very Good.


3. MRCEM (UK): Membership of Royal College of Emergency Medicine, United Kingdom.
There has been lot of confusion regarding this. So let's make few facts clear.
1. This is NOT an Indian qualification. This is awarded by RCEM, UK.
2. It is recognized by MCI as an additional postgraduate qualification and can be added to your certificate in state medical councils (I personally know many people who have registered their qualifications)
3. You can apply for faculty positions in medical colleges with MRCEM as per the latest notification by MCI. You can find it here: https://www.mciindia.org/documents/e_Gazette_Amendments/TEQ-11.03.2017.pdf
(I don't have first hand info about anyone who have done so yet - So unsure of the process involved)
4. You can get job in any hospital after MRCEM easily.
5. You are eligible for working in UK/Ireland and/or undergo higher specialty training in UK towards FRCEM. (You are exempted from PLAB). FRCEM is recognized in Australia as well.

Note :  With MRCEM in your pocket, you are eligible to work as a Registrar in UK, NOT as a consultant. However, in India - you will be offered consultant posts by many hospitals after you pass MRCEM exams. MRCEM is half way through training. Emergency Medicine training lasts for 6 years in UK and FRCEM is required before you start working as a consultant.  Here is UK training pathway in Emergency Medicine: 



6. Do you have to be in a specific residency or training program to attempt MRCEM exam? The answer is NO. You need to have the evidence of structured training/experience in EM and allied specialties as per RCEM requirements - Emergency medicine, Intensive Care medicine, Anesthesia, Acute/Internal medicine (For roughly 3 years) and you can attempt the exam.
Follow the RCEM link for minute details of exams and everything else: http://www.rcem.ac.uk/

7. Is the exam easy? Hell no! You would know this if you speak to the people who have either passed or attempted the exam. Also if you look at the pass percentage of the exam you will have a fair idea how difficult the exam is.  The pass percentage in each part is roughly around 25-30. (The exam has 3 parts - A, B, C - Recently changed to FRCEM primary, intermediate and OSCE - Will not get into the details and add to the confusion - Refer website for finer details)

8. What's the Apollo connection with MRCEM ?
This has always been a longstanding doubt of many. Simple. Apollo was the first in the country to collaborate with RCEM and start the MRCEM exams in India and started a structured training program in EM providing training to pass MRCEM back in 2005 (During a time when EM was not even a MCI recognized specialty in India), pioneering the development of EM in India.
Apollo runs a structured 3 year EM residency program training you for MRCEM.
So MRCEM exams are usually held at Apollo hospitals. Recently there have been few other centers like Max Hospitals, Delhi.

9. So is it mandatory to get training in Apollo to be eligible for MRCEM ?
No. Absolutely not. College (RCEM) doesn't mind where you do your training from as long as you are competent and can show the evidence of same neither they RECOMMEND any specific training program.
So basically you can write MRCEM after MRCEM residency in Apollo, DNB EM, MD EM, MEM, or not enrolling yourself into any of the courses per se and just gaining the necessary experience/training in the specialties mentioned above.

10. So is doing residency in Apollo useless if my aim is doing MRCEM ?
Definitely not! They have a very good EM dept. where there are seniors/registrars/consultants who have completed MRCEM who can guide you. It's a JCI accredited hospital and you have defined protocols. You have a decent patient load and fair amount of independence. You are rotated through different specialties ALMOST as per the RCEM curriculum. They can train you before the exam. Having expert guidance is the key to pass MRCEM apart from having good training and experience. + The EM culture in Apollo is good and you will have your identity as an emergency physician. (This is only with Hyderabad where I worked and Chennai where I have few of my friends - I can't comment about other Apollo Centres)
Having said that just because you have enrolled for the residency program doesn't automatically mean that you will pass MRCEM exam. You are not joining a 'course' where you will be spoon-fed. You will have to earn it!

11. Can I join any other hospital, college without enrolling into a course/training program and still clear exam ?
Well, nothing is impossible. You CAN do that as well provided you have a very good guide and you exactly know what you are doing. There are people who have done that as well. So it is completely up to you! Thinking out of the box is a core quality of an emergency physician! But you have to judge how much out of the box!

12. What in UK after MRCEM ?
Most of the UK training programs run for 6 years (ST1 - ST6). So you will be entering as a middle grade registrar (ST3/4 level) after MRCEM. You can complete rest of the years in UK and can also apply for subspecialty training in Pediatric EM and Prehospital EM. You can also opt for dual accreditation in ICM which is for 6 years post MRCEM (FFICM). (Again, not getting into the different pathways after MRCEM for higher specialty training - Refer to college website for the same)

Downsides:
- Some of the corporate hospitals with training programs for MRCEM pay very (very) less! (So you will be devoid of money for 3 years and the restaurant owner will be singing 'Abhi na jao chodkar ye bill abhi bhara nahi'). Some of the hospitals do not pay residents for first 6-8 months of training (Zero – Yeah! You will be doing some charity work for the poor and needy corporate hospitals.....Smirk, smirk!)
-No leaves for the entire 3 year (almost 1100 days) duration except for the post night offs. (Note that this is a common problem with most courses and not specific to this)
- Training can become dull/not-so-happening sometimes especially if there's shortage of staff.
-The place you choose for training is extremely important. Especially if it is not a structured training program – High chances of losing focus, getting lost and getting discouraged by ill informed peers, colleagues and 'experts' from other specialties.
-There are only a handful of MRCEM qualified doctors in India. Choosing the right guide in a right hospital out of a training program might be a tedious task.

Bottom-line: You need to find a very good hospital and have adequate training/experience to clear MRCEM. A good guide/team is equally important. Exam is definitely not easy. You will have to earn this qualification. Scope: Very good! MRCEM opens up many doors for work/training in India and abroad.
PS: One other major downside would be explaining MRCEM to everyone after you are half dead explaining what emergency medicine is.  Whenever that new uncle goes "Beta, kya kar rahe ho aajkal?" You will be like 'Maar daalo mujhe...Maar do!'

4. MEM (Masters in Emergency Medicine):
MEM (Masters in Emergency Medicine) is a three year course run by 2 societies - George Washington University, USA and SEMI - Society for Emergency Medicine, India. Probably this is the most 'controversial' of them all.
Before I start, I'm making it clear that I'm not jumping into the argument of whether or not these societies can give masters degree , universities act, it's just a certificate, should it be called something else etc. Etc. - I'm not a legal expert. Period. Now that these courses are being run and people have enrolled into them let's see how can they be assessed by a trainees perspective.

The overview of MEM programs:
1. Are they recognized by MCI ?
A: An absolute NO.
2. Is the GW MEM recognized in USA?
A: No again. A big NO.
3. Is it recognized in UK?
A: NO man, NO! Nooooo!
4. Can you get a job after MEM ?
For now, of course you can get a job with fairly good pay as there's a shortage of doctors to man the EDs. But future is unclear.
5. Can i write MRCEM after MEM ?
Yes. Of course you can, like anyone else with similar experience. But your MEM tag has nothing to do with MRCEM exam!
6. So is MEM completely useless ?
Well, No! Again it's unfair to give such a blanket statement. MEM programs have a good curriculum (Although not all the centers adhere to it or have a notable training program). There are quite a few centers running MEM programs with very good training which produce very good EM physicians and also high success rate in MRCEM. (Example: MIMS Calicut, KDAH Mumbai, MaxCure Hospitals Hyderabad. There may be other hospitals which have good training programs and these are just examples of hospitals I'm aware of which have good training as per few friends and colleagues who had worked there).
Many of the courses conduct regular classes/academic sessions, some even with overseas faculty.
7. So are MEM trained doctors are all incompetent ?
No. 'Unaccredited program does not equal to incompetent trainees' and vice versa (I hate blanket statements, please clinically correlate - Also remember Sharmaji's son's story)

Downsides:
- Fee for most of GW MEM courses are high.
- Although the training in some hospitals is good, ultimately everything boils down to success rate in MRCEM! So the importance of MEM as a standalone qualification is minuscule especially with it's 'Unrecognized' status.
- Many hospitals use MEM as a way to get cheap labor - To prevent understaffing of their EDs and ICUs without actually training them and also underpaying them - Which definitely is a major concern.
- Many people opt for it because they are not able to get into anything else. (Ease of entry). Which again is detrimental to the specialty.
- Most of the MEM programs are advertised saying they are eligible to write MRCEM after MEM which is of course true but what is the role of MEM per se needs to be seen. Only time can tell the answer ?!
Bottom-line: Joining MEM might not be a very bad idea if you like the training in a particular hospital running MEM course and IF THEY ALSO (ACTUALLY) TRAIN YOU FOR MRCEM.
'Only MEM' is probably like a Limbo in Inception! You are nowhere! (At least in the present scenario)

Few words about the nomenclature war:
The cause for this confusion is complex. It may range from personal interests to governmental insufficiency in uprooting the corruption in the system + the mismatch between supply and demand and everything in between – Corporate greed, personal agenda, petty politics, lack of manpower, funding, infrastructure and the extremely complex system of Indian healthcare. Frankly I don't have one answer for this neither can I think of one single solution for this. But definitely conflict and 'rational thinking loss' are detrimental to the growth of EM as a specialty!

There has been a lot of buzz in the social media after few reports were published in prominent newspapers about EM qualifications in India. The newspaper articles although highlighted few problems, it failed to make an unbiased approach and made it appear as if everything is right with the MD and DNB courses and everything else is wrong with the other courses. Many polarized opinions were being circulated with everyone claiming how certain degrees/qualifications are all good and how others are all bad. This is just an honest attempt to provide an unbiased approach towards these qualifications which might help an aspiring EM doctor!

I hope there will be less chaos in the days to come and hope that the Governmental bodies and non-governmental professional bodies work together instead of working against each other so that EM grows further as a specialty in India. Hope there will be common ground of assessing the competencies and logical conclusion to this without jeopardizing the aspirations and dreams of people wanting to take up Emergency Medicine. In EM we trust :)


Summary:
A. There are different ways of achieving something. No one path is perfect for everyone. So what do you want to choose?
B. DO NOT believe people giving blanket statements about things/issues. It's not just black or white!
C. Don't even believe this article. Do your own critical appraisal!!!
D. Visit the college/hospital, speak to residents/trainees, consultants before joining any program. Know what you are doing and what you want to be!
E. Personally, depending upon all the above info, I would rank the qualifications as follows:
1)DNB EM 1)MRCEM  2)MD EM  3) MEM

References:

Disclosures and Conflict of interest: I have done my 3 years EM residency from Apollo Hospitals Hyderabad and have completed MRCEM. So there might be a slight positive bias towards Apollo in the Article although a conscious effort has been made to avoid the same. The views expressed here are the opinion of author only.


Author:
Dr. Apoorva Chandra
MBBS, MRCEM(UK)
Specialist Registrar – Emergency Medicine
Northwick Park Hospital

London, United Kingdom