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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, 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

Dysmotiliy
  • 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

Symptoms
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. 


Management

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:
https://coreem.net/podcast/episode-74-0/

Posted by:

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

     @EMDidactic






  

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
     England

     @EMDidactic