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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, June 27, 2016

Salbutamol induced hyperlactaemia

Case


24/F with a history of Asthma presented to the ED complaining of shortness of breath that progressively got worse over the past couple of days in-spite-of increased use of inhalers. She has been intubated twice before due to asthma exacerbations. She never smoked and denied having any pets. 



In the ED, she received prednisone and multiple doses of albuterol nebulizations. Physical exam showed mild distress, BP 110/70, PR 110/min RR 28/min. She was able to talk in full sentences and was saturating 100% on 2 liters. Her best peak flow was reportedly 400, and she only did 150. She had bilaterally decreased air entry and significant expiratory wheezing. 

ABG on arrival showed a lactate level of 3 with a peak flow of 220. With treatment, in spite of an improvement in her peak flow to 300, she looked more tachypneic and lactate level increased to 5.5. Rest of the labs and CXR were normal.





Discussion

Salbutamol/ Albuterol is a β2 agonist used for bronchodilation in asthma. Salbutamol causes lactic acidosis by a combination of factors, but the exact etiology remains unclear. It is probably due to its metabolic effects. By creating a hyperadrenergic state it enhances glycogenolysis and gluconeogenesis, leading to more glucose, enhanced glycolysis, and pyruvate production. At the same time, enhanced lipolysis and increased free fatty acids inhibit pyruvate dehydrogenase enzyme, preventing pyruvate from entering the Krebs cycle. This causes pyruvate reduction to lactate.







Reports of lactic acidosis induced by high dose beta agonists used for tocolysis and bronchodilation have been described in obstetric and asthmatic patients. 


What are the types of Lactic Acidosis?

Type A Lactic Acidosis occurs when oxygen delivery to the tissues is compromised. 

Type B Lactic Acidosis occurs when either lactate production is increased or lactate removal is decreased without obvious oxygen delivery problems. It occurs due to increase in both endogenous and exogenous catecholamines. Enhanced β2 receptor activation leads to increased glycogenolysis, gluconeogenesis, lipolysis and ultimately to increased conversion of pyruvate to lactic acid. Concurrent corticosteroid use may enhance the beta receptor sensitivity further potentiating the lactic acidosis. 

Conditions associated with type B lactic acidosis include inborn errors of metabolism (pyruvate dehydrogenase deficiency), systemic disorders (liver failure), and medications (ethanol, metformin, and corticoids). It has also been postulated that endogenous (distress) or exogenous (drugs) adrenergic stimulation may be associated with increased conversion of pyruvate to lactate. 


What are the common blood gas findings in Acute Asthma?
The common metabolic disturbances seen during an acute attack are respiratory alkalosis, followed by respiratory acidosis as patients get tired of breathing.


What are the possible causes of lactic acidosis in Asthma?
1. Pulsus paradoxus and intrinsic PEEP decrease cardiac output and venous return
2. Production of lactate by overworked respiratory muscles
3. Hyperadrenergic State (Beta 2 agonist-induced)


Why is it important for us to know about this?
Albuterol induced lactic acidosis creates a paradoxical situation where there is enhanced bronchodilation but worsening tachypnea as a result of compensation for metabolic acidosis. Acidosis results in hyperventilation which could be mistaken for poor response to treatment. Physicians might misinterpret this situation as worsening respiratory failure and give more albuterol, creating a vicious cycle and ultimately leading to respiratory failure. 

Serial peak flow measurements and examination is the ideal way to identify this situation.


Take Home:
While treating asthmatic patients for severe bronchospasm, when lungs sound clear following treatment but tachypnea persists, suspect albuterol-induced hyperlactatemia. 


References:

  1. Dodda, Venkata R., and Peter Spiro. "Can albuterol be blamed for lactic acidosis?." Respiratory care 57.12 (2012): 2115-2118.
  2. Stratakos G, Kalomenidis J, Routsi C, Papiris S, Roussos C. Transient lactic acidosis as a side effect of inhaled salbutamol. Chest. 2002 Jul;122(1):385-6
  3. Stratakos G, Kalomenidis J, Routsi C, Papiris S, Roussos C: Transient lactic acidosis as a side effect of inhaled salbutamol. Chest 2002; 122: 385–6Stratakos, G Kalomenidis, J Routsi, C Papiris, S Roussos, C 
  4. Prakash S, Mehta S: Lactic acidosis in asthma: Report of two cases and review of the literature. Can Respir J 2002; 9: 203–8Prakash, S Mehta, S 

Author:

              
     Lakshay Chanana
     @EMDidactic
                                                        


 


Monday, June 20, 2016

History Taking - Revisited

From the moment we start interacting with patients as medical students, we are always taught that a good history and physical is of paramount importance to clinch a diagnosis. Faculty from medical schools across the globe, emphasise on this point over and over in an attempt to mould the thought process of students. But in modern day scenario, most of you would agree that the pendulum has swung way too far towards labs and imaging. Sometimes, history and physical is cut short or even completely skipped due to over-reliance on labs. 



I think labs certainly form an important component while evaluating patients, but a balance needs to attained between labs and history/physical. Work up needs to individualised based on presentation, order of differentials i.e every chest pain does not need D-Dimers, CT Pulmonary Angiogram, Cardiac Cath and Endoscopy!




Let us remind ourselves the key components of history taking. This of course, comes in addition to communication skills which are learned over time. Read more on Medical Interview communication skills here.






If done fluently, this elaborated history take anywhere between 10-15 minutes. However, in the ED we rarely need to ask all this questions to all the patients. ED history is focused depending on the chief complaint and also due to time constraints. So this format needs to be gauged based on every individuals chief complaint. For instance, don't dig into getting a detailed sexual history in a 75/M with acute chest pain but do a thorough sexual history in a 24/F with lower abdominal pain or vaginal discharge.


The key is starting with the Chief Complaint, if there are a couple of them then ask the patient which one makes him more concerned. Following this do the Past History (Medical, Surgical, Sexual, Family, OBGYN, Social, Sexual and Allergies) and then ask YES/NO type of questions in the Review of Systems (ROS). One you are through this, do a quick and focussed examination. Now, when you probably have a few differential diagnosis in your mind, order the tests  based on ruling in or ruling out (to a certain extent) these differentials. 

Also remember that while working in the ED, you often treat the symptoms and a suspected diagnosis (awaiting labs). 


Take Home:
  • No lab test/imaging can replace history and physical examination 
  • Follow the sequence (History-->Physical-->Differentials-->Labs)
  • ED history is focussed, based on the chief complaint

Author:

              
     Lakshay Chanana
     @EMDidactic
                                                        


 

Monday, June 13, 2016

Welcome to Emergency Medicine by Rahul Patwari

Over the last decade, EM has become incredibly popular among medical graduates in India. But quite often, students begin ED rotations without a formal induction session. Here are a few quick videos to understand how things work in Emergency Medicine and how Emergency Physicians think, by Rahul Patwari. This video gives a sort of introduction to Emergency Medicine before interns/residents begin working in the ED.

Welcome to EM


         



Clinical Thinking in EM - 1

                                          



 Clinical Thinking in EM - 2

                                          


For more such videos, subscribe to Dr. Patwari's YouTube channel

Thanks to Dr. Patwari (@rahulpatwari) for supporting our site!

For more on EM induction, Check out this link on how to present a case in the ED and If you want to know Why do I keep falling in love with EM? "OVER AND OVER", click here!

Monday, June 6, 2016

Selfie Fever: What are we up to?






                  
  • Avoid taking selfies from a height, on a bridge, in the vicinity of vehicular traffic, during thunderstorms, at sporting events, and where wild animals are in the background.
  • Travel medicine fellows should now routinely counsel travellers about responsible self-photography during international travel and should also include this advice in printed material given to the patient.  
  • Most importantly, each one of us needs to recognise this issue and behave in a  responsible manner.

References:
  1. https://en.wikipedia.org/wiki/List_of_selfie-related_injuries_and_deaths
  2. https://www.washingtonpost.com/news/worldviews/wp/2016/01/14/more-people-die-taking-selfies-in-india-than-anywhere-else-in-the-world/
  3. http://timesofindia.indiatimes.com/tech/social/India-had-the-most-selfie-related-deaths-in-2015-Report/articleshow/50593587.cms
  4. The 'selfie' phenomenon: reducing the risk of harm while using smartphones during international travel Flaherty GT, Choi J. J. Travel Med. 2016; 23(2): e026. 
  5. http://connecticut.marketing/2015/07/russian-selfie-guide-in-english/

Author:

              
     Lakshay Chanana
     @EMDidactic