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I completed my medical school and background EM training from India (Christian Medical College, Vellore and Apollo Hospitals, Hyderabad) where I worked for 4 years. Following this, I devoted (with all my heart) about 1.5 years to do US Medical Licensing Exams. My stint towards an EM Residency in States did not work but it took me to places and it has been quite a journey. I then relocated to London, England to work as a Registrar (Non-Trainee) in A&E. This gave me an opportunity to better understand NHS, EM training pathways and more importantly the EM Mindsets in the United Kingdom. 

Currently, I am pursuing Higher Specialist Training in Emergency Medicine at South East Scotland Deanery where I have the honour and privilege of training under some of the most innovative brains in the field of Emergency Medicine. Over the past few years, I have realised that LEARNING and UNLEARNING (which can be challenging!) is equally important to deliver cutting edge care to our patients.And through this blog, I aspire to disseminate knowledge, assist trainees with exams and stay up to date with contemporary EM literature. I have always been an avid FOAMed supporter because FOAMed has always played an indispensable role during my training. 

Lakshay Chanana
ST4 EM Trainee 
Edinburgh, Scotland

Monday, September 25, 2017

Cocaine Toxicity

Cocaine is one of the most commonly used recreational drug. It is both a CNS stimulant and a local anaesthetic.Its clinical effects and toxicity are due to sympathetic nervous system stimulation. Cocaine can be used topically, swallowed, or injected IV. 


Cocaine is metabolized by plasma cholinesterase. Therefore, deficiency of this enzyme may predispose affected patients to life-threatening toxicity.  Central effects of cocaine are mediated by enhancement of excitatory amino acids and blockade of presynaptic reuptake of norepinephrine, dopamine, and serotonin. The excess of neurotransmitters at postsynaptic receptor sites leads to sympathetic activation, producing a characteristic toxidrome of mydriasis, tachycardia, hypertension, and diaphoresis, dysrhythmias, seizures, and hyperthermia. 

Like other local anesthetics, cocaine also inhibits conduction of nerve impulses by blocking fast sodium channels in the cell membrane. This can lead to QRS widening and QT-interval prolongation. 

Systemic Effects
  • Dysrhythmias (Na/K Channel Blockade - Sinus Tachy, Wide QRS, Prolonged QTc, Rightward Axis, Brugada Pattern, Takotsubo Cardiomyopathy)
  • Myocarditis
  • Acute coronary syndromes
  • Aortic rupture and aortic/coronary artery dissection
  • Cocaine-induced chest pain (Coronary Vasospasm, also hastens atherogenesis through increased platelet aggregation, thrombogenesis)
  • Seizures
  • Stroke (ischemic and haemorrhages)
  • Hypertension
  • Spinal cord infarction
  • Cerebral vasculitis
  • Intracranial abscesses
  • Crack dancingChoreoathetosis and repetitive movements due to dopamine dysregulation. 
  • Blindness (central retinal artery occlusion)

Other effects
  • Pulmonary haemorrhage
  • Pneumonitis, Asthma
  • Pulmonary edema
  • Acute Lung Injury
  • Thermal uvulitis 
  • Bowel schema and necrosis
  • Splenic infarctions
  • Rhabdomyolysis and AKI 
  • Renal infarction 

Differential Diagnosis of Sympathomimetic Syndrome
  • Anticholinergic Syndrome
  • Serotonin Syndrome
  • Neuroleptic Malignant Syndrome
  • Alcohol Withdrawal
  • Sepsis and CNS Infections
  • Hypoglycaemia, Metabolic (Electrolyte Issues)
  • Thyrotoxicosis
  • Pheochromocytoma
  • Psychosis
  • Heat Stroke 

  • Benzodiazepines are the drugs of choice for sedation
  • Antipsychotics increase QT prolongation and increase risk of ventricular dysrhythmias
  • Treat Cardiac Chest Pain with aspirin and nitroglycerin, CCBs and reperfusion therapy if needed.  
  • Use of β-adrenergic antagonists (“β-blockers”) in the management of cocaine-associated myocardial ischemia or infarction is controversial. 
  • Sinus tachycardia - Rx with sedation, cooling, and intravenous fluid rehydration 
  • Reentrant supra ventricular tachycardia /Fast atrial fibrillation or flutter - Rx with CCBs
  • Wide-complex tachycardia - Rx with sodium bicarbonate (do not alkalinize above a pH of 7.55). Although Lidocaine is also a Na Channel blocker, it may be considered for use in refractory arrhythmias.
  • Torsades de points - Rx with Magnesium, lidocaine, and overdrive pacing.
  • Hypotension/Persistent Arrhythmias - Intravenous lipid emulsion should be considered in this scenario.
  • Severe hypertension - Rx with sedation or GTN drip or Phentolamine
  • Rhabdomyolysis - IV Fluids
  • Seizures - BZD, Phenobarbitone (Do not Rx with phenytoin which may worsen Na Channel Blockade)

  1. Zimmerman JL: Cocaine intoxication. Crit Care Clin 28: 517, 2012. 
  2. Phillips K, Luk A, Soor GS, Abraham JR, Leong S, Butany J: Cocaine cardiotoxicity: a
  3. review of the pathophysiology, pathology, and treatment options. Am J Cardiovasc Drugs 9: 177, 2009. 
  4. Lange RA, Cigarroa RG, Yancy CW, et al: Cocaine-induced coronary artery vasocon-striction. N Engl J Med 321: 1557, 1989. 
  5. Hollander JE, Hoffman RS: Cocaine-induced myocardial infarction: an analysis and
  6. review of the literature. J Emerg Med 10: 169, 1992. 
  7. O’Leary ME, Hancox JC: Role of voltage-gated sodium, potassium and calcium channels in the development of cocaine-associated cardiac arrhythmias. Br J Clin Pharmacol 69:427, 2010. 
  8. Yap YG, Behr ER, Camm AJ: Drug-induced Brugada syndrome. Europace 11: 989, 2009.
  9. Arora S, Alfayoumi F, Srinivasan V: Transient left ventricular apical ballooning after cocaine use: is catecholamine cardiotoxicity the pathologic link? Mayo Clin Proc 81: 829, 2006. 
  10. Rangel C, Shu RG, Lazar LD, Vittinghoff E, Hsue PY, Marcus GM: Beta-blockers for chest pain associated with recent cocaine use. Arch Intern Med 170: 874, 2010. 
  11. Jakkala-Saibaba R, Morgan PG, Morton GL: Treatment of cocaine overdose with lipid emulsion. Anaesthesia 66: 1168, 2011. 

Posted by:

     Lakshay Chanana
     Speciality Doctor
     Northwick Park Hospital
     Department of Emergency Medicine


Friday, September 22, 2017


Yes, the exam is back. And it shall be over sooner than you can imagine. Well one thing is common for most of students – the Uncertainty. No matter how well they have read.  Also if someone would question them about their preparation at this juncture they will hate you for simply asking.

In January, 2017 I had written a post on my experience with FRCEM SAQ intermediate exam. Of late, I have been getting multiple mails and phone calls from exam going candidates asking how to prepare, what to read and so all. Yes, I may have cleared this exam almost a year ago but totally empathize with all the following statements – “My mind has gone numb” “I keep forgetting everything” “How will I revise” and so on…

One week to go. Maybe you’re the guy who has read and revised the entire course OR maybe you’re the one who is starting today. Either way all any candidate wants is to pass this exam. This is the crash zone. Either you make it or break it. Any panic, anxiety or worries are detrimental. The main reason of this is thinking about the exam result and what catastrophe would beckon if you were to fail! All these thoughts will make you anxious and if with that thought process you try to study you will feel frustrated because ‘nothing is going inside your head!’ and your mind wants to take a break to relax. This loop of worry, anxiety and breaks continue and the day gets over. Similarly more days go by and when it is just 24hours before the exam, you realize YOU COULD HAVE prepared a lot better IF ONLY YOU HAD A WEEK!

So, now, you do have AN ENTIRE WEEK! That’s a whole lot of time if you plan correctly and simply focus on the task to complete in the NEXT ONE HOUR!
Let’s change our mindset from what will happen to what is to be done. Let’s begin. Here is an Eight pointer for you:

1.     Make a promise to yourself now – That you will not think of the result of the exam. Passing or failing is not in your control. Your result entirely depends on WHAT YOU DO NOW RATHER WHAT YOU WISH should happen.

2.     PLAN. IF PLAN fails – REPLAN. Exam preparation in last week is like a busy shift in the ED, your plans of treatment and disposition may work sometimes and most of the times they won’t. You don’t leave your shift because it got crazy. You complete the shift, tackle everything, come what may.  Therefore if you slack in your plan, don’t worry, replan your day from that moment and start doing. Remember every second you waste in worrying makes your brain tired and less receptive to newer information.

3.     Adjust your shifts. Take leaves if possible. Can’t elaborate on that further.
4.     Take a brand new notepad/folder - Name it - ‘LAST MOMENT FOLDER’. You may add your old notes but I insist you write all new . (For that matter I even brought a new OHEM as my old one was all colored and gave me a false impression that I have read everything). The new notes/ folder will be based on your current status where you know what your strengths and weakness are. So make a folder and keep adding nuggets of information to it. Let it be a live tracker of your week and store all important stuff out of whatever you read. It doesn’t have to be bulky or comprehensive. The aim is to identify the key points that that you would want to revise on last day if you had only 2-3 hours left. Keep it 24x7 with you.  So here are few suggestions for the ‘Last moment folder’ - (Filter the items according to your requirements)

a.     Management of every acute or emergency condition (in no more than 3-4points - This helps in answering in exam also) - Write the interventions. Write the Drugs with name - dose - route. (Believe me! This is where most people falter)
b.     Formula/ Calculations like Anion Gap, Sodium correction, Calcium correction, A-a gradient etc with their normal values
c.     ECG changes in various conditions
d.     Classification and scores
e.     Definitions
f.      Pediatric doses and NICE guidelines on pediatric traffic light system
g.     Conditions/ signs with specific names

5.  Use GOOGLE images search- Since most of the questions in the exam are image based, it is suggested that with every condition you read, keep searching it’s images. The first page of Google image search will give you the most representational pictures and it is highly possible that you get one of those images in the exam. Also it helps developing a visual memory that stays longer.            

6. Now the question comes – HOW TO PLAN? Well there is no ideal way. Every person have their own methods. Considering the exam day as day 7. Let us divide the 6 days in hand into 3 segments - a) 72hrs - Days 1-3  b) 48 hrs - Days 4,5 c) 24 hrs - Day 6. Define your goals for each aforesaid segments. Next,  I’d suggest divide these segments into 6 hour intervals. Have a specific target for each 6 hours. Plan your breaks and naps accordingly. This will keep you focused. So if the exam date is 28th September - The week starts 22nd September. 
A) Days 1-3 (22,23,24th September) - Plan to simply read through entire syllabus according to the topics in the curriculum and identify key points needed for revision. Since it’s the last week I would not go for bigger reference textbooks, rather read from books and sources which I am familiar with and are exam oriented viz. Oxford Handbook of Emergency Medicine and Acute Medicine, Few NICE guidelines, SCORES. Keep 6 hourly targets for example  - Surgical and Environmental emergencies in 6hours. While reading keep marking ‘Q’ whatever you feel is a possible question. (Well sometimes there were more than 20 Qs marked on the page!). None the less, it will help you in later stage.  Also keep writing the points which needed to be revised and add them to your ‘last moment folder’.       
B) Days 4-5 (25,26th September)- The REVISION - These 48 hours revise the highlighted texts or the ‘Qs’ you have marked in your books. Keep adding and updating your ‘Last moment folder’.  If you have some topics pending (probable) and time left (improbable) then try covering them as well.
C) Day 6 (27th September)- This is the last day before exam. Plan your day in 2nd hourly intervals. DO NOT read anything new. Just read you ‘Last minute folder/ notes’ and the topics. You have to ‘by heart’ all important stuff.
D) Day 7 (28th September)- Day of exam. Preferably do not keep anything to read today. If you still have to, then no more than 1-2 hours with only pre-planned topics from your revision folder. Don’t read new stuff neither do haphazard studying, this will drain you off energy.
 Nobody gets a good sleep before an important exam. So don’t worry about it much. Have a decent breakfast. Keep nuts or chocolates with you when going for exam (although you’ll be provided refreshments). Stay hydrated but pee before the exam. For further details of the way exam is conducted and how to manage your time, kindly refer to my previous post in January.

7. Online questions - Use them to test yourself - Assess your time management. Use these questions to streamline your answers.

8. Breaks and naps - Take effective breaks of no more than 2hours per 6hour. Do not be away from reading for more than 12hours. The break should recharge you and not leave you with guilt. 

Dear Friends, in the last week, the objective is to cover entire syllabus and revise it effectively. There may be different way to prepare for this exam. I just shared with you what I would do if it were 7days to the exam. I wish you the best. Stay Calm, Stay focused.

Let me know if this post helped. Cheers! :)

Written by:
Dr. Akshay Bhargav MBBS, DEM, MRCEM

Akshay is an emergency medicine enthusiast. Originally from Kanpur, he did his graduation from Kasturba Medical College, Manipal and his post graduation residency in Emergency Medicine from Apollo Hospitals, Hyderabad. He Loves teaching via simulation methods. His dream is to spread emergency medicine awareness among masses and improving standards of ED care in the country. As a student has always hated examinations but thankfully chose never to give up.

Monday, September 18, 2017

Firing the Esophagus - GERD in ED

GERD is often listed as a part of Chest Pain differentials in ED. It is caused due to the reflux of gastric contents into the oesophagus and can cause a multitude of symptoms and it can be challenging to differentiate from ACS. A weak lower esophageal sphincter is frequently responsible for reflux. However, asymptomatic reflux several times a day is a normal physiologic phenomenon. 

Causes of GERD

  • Achalasia
  • Scleroderma
Prolonged Emptying
  • Anti-cholinergics
  • Gastric Outlet Obstruction
  • Diabetic Gastroparesis
  • Fat rich diet
Low LES tone
  • Ethanol
  • Caffeine, Chocolate
  • Tobacco Smoking
  • Medications (CCBs, Nitrates, Progesterone, Oestrogen)
  • Pregnancy

Pain and discomfort with meals indicate GERD. Symptoms might be exacerbated with a head-down position or an increase in intra-abdominal pressure. and are transiently alleviated by antacids. GERD may be accompanied by diaphoresis, pallor, and nausea and vomiting which makes it hard to differentiate from cardiac pain. 
  • Heartburn
  • Diaphoresis, pallor, and nausea and vomiting (Always rule out Cardiac etiology)
  • Odynophagia, dysphagia, Acid regurgitation, and hyper-salivation (Water brash) 
  • Asthma exacerbations
  • Sore throat and other ENT symptoms
  • Dental erosions, gingivitis, halitosis, vocal cord ulcers and granulomas, laryngitis with hoarseness and repeated throat clearing
  • Chronic sinusitis
  • Chronic cough
Long standing GERD may lead to strictures, dysphagia, and inflammatory esophagitis.  

Radiation into both arms is rarely seen in reflux, whereas it may be present in approximately one quarter of patients with ischemic heart disease. 


GERD is a very common problem. ED management focuses on ruling out the life threats, proving symptomatic relief and arranging follow up care. 
  • H2 Blockers or PPIs (PPIs are more effective than H2-blockers in eliminating symptoms and healing mucosal damage)
  • Antacids
  • Pro kinetics 
  • Lifestyle advice (Weight loss, avoid ethanol, caffeine,nicotine, chocolate, fatty foods, sleep with the head of the bed elevated, and avoid eating within 3 hours of going to bed at night)
  • Follow up care (esophageal pH monitoring, an upper GI radiographic series, esophageal manometry, or esophagoscopy may be necessary, especially for patients who fail to respond to all of the preceding measures

Further Reading:

Posted by:

     Lakshay Chanana
     Speciality Doctor
     Northwick Park Hospital
     Department of Emergency Medicine



Monday, September 11, 2017

EtOH intoxication

Ethanol is the one of the most commonly abused drug in the world. Mishaps generally happen due to secondary injuries after intoxication. We all see frequent attenders in ED who visit us almost every weekend and it is easy to miss underlying potentially life-threatening diseases if we fail to follow a systematic way to evaluate them.

Alcohol Metabolism
Ethanol is a CNS depressant that enhances the inhibitory neurotransmitter GABA receptors and blockade of excitatory NMDA receptors. Because of the phenomenon of tolerance, blood ethanol levels correlate poorly with degree of intoxication.  At low concentrations, ethanol metabolism follows first-order kinetics, but as concentrations rise, metabolism switches to zero-order kinetics i.e. a fixed amount is metabolised per unit of time. Rates of elimination from the blood vary between 20-30 milligrams/dL/h.
The legal limit to drive a vehicle varies in different countries. UK, Canada and the United States state 80 mg/dL as the legal definition of intoxication for the purposes of driving motor vehicles whereas in India, the limit is 30mg/dL. 

 Clinical Presentation
Lethargy, Drowsiness, Disinhibition, Euphoria, Agitation and Combativeness are classical clinical features. However, severe intoxication may present with slurred speech, nystagmus, ataxia, and decreased motor coordination and this can be hard to differentiate from Wernicke’s. Treat them with fluids if they are tachycardic (reflex tachycardia due to peripheral vasodilatation). Fever should prompt workup for sepsis and possible Delirium Tremens. Ethanol ingestion may also cause hypoglycemia, due to poor glycogen reserve, poor oral intake and reduced gluconeogenesis.

Potential Mimics and co-existing conditions
  • Encephalopathy (Hepatic, Uremic, Septic)
  • Hypoglycaemia
  • Traumatic Brain Injury (Subdural)
  • Stroke
  • Seizure
  • Wernickes
  • Concomittant drug ingestions
  • Dyselectrolytemia (HypoNa, HyperNa, HyperCa)
  • Alcoholic Ketoacidosis
  • Hypothermia
  • DKA
  • Myxoedema
  • Psychosis
  • Alcoholic Hepatitis and Pancreatitis

ED Management
Performing a detailed physical examination is paramount (Speech, Cranial Nerves, Gait, Nystagmus, GCS, Cerebellum, Evidence of trauma, Abdomen exam) to avoid missing co-existing conditions. Fill the gaps in your history via paramedics, by standers. Usually, uncomplicated intoxication improves within a few hours but if they don’t get sober or worsen then begin evaluation for other causes of altered mental status.
If history and exam are benign then investigations are of limited benefit. At least, obtain a bedside glucose level or a venous blood gas. Acute intoxication may be associated with mild metabolic acidosis, but a significant HAGMA suggests the presence of lactic acidosis, ketoacidosis, or methanol or ethylene glycol toxicity. Ethanol blood levels are not required unless there is a diagnostic dilemma but many prefer to do it anyways to ensure documentation. 
Most physicians agree that observation is the way to go until they are sober. Manage symptoms and beware of hypoglycemia. The classical teaching of Wernicke’s encephalopathy being precipitated by prolonged sustained administration of IV carbohydrate does not hold true and currently there is no evidence that a single dose of IV glucose can cause Wernicke’s.  Otherwise, majority of them do NOT need Pabrinex but administer if you suspect Wernicke’s. Additionally, bolus IV fluids do not help to attain sobriety any earlier. Metadoxine is used in some countries to enhance the metabolism of ethanol and accelerate recovery.
Take Home:
Simple ethanol intoxication needs ED observation until sober. Admit if they are suicidal, homicidal or psychotic. Always try and arrange appropriate transport for them and discharge in the care of a responsible companion.

Posted by:

     Lakshay Chanana
     Speciality Doctor
     Northwick Park Hospital
     Department of Emergency Medicine