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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
drlakshayem@gmail.com

Friday, March 8, 2019

Septic Arthritis

Septic arthritis is a destructive disease process classically presenting as a red, hot and swollen joint. The disease has a bimodal incidence, which peaks in young children and adults over age 55 years. Unfortunately, septic arthritis is not always easy to diagnose and  presentations may be subtle without classical signs, symptoms, or laboratory markers. It remains one of those cannot miss diagnosis which are always fraught with fear. Therefore, the dictum is "Red Hot Swollen joints should be tapped" to r/o Septic Joint.   Fluid is then sent for Gram Stain, C/S, White Cell count and Differential count, and Crystal analysis. 

Routes of Spread: Common routes of spread is hematogenous followed by direct inoculation (trauma or localised spread from a surrounding soft tissue infection)

Common Joints - Knee>Hip>Shoulder>Elbow


Risk Factors for Septic Arthritis (More abnormal joint, more likely Septic Arthritis)

  • Bacteremia/systemic infection
  • IVDU (may have sternoclavicular and sternomanubrial joint involvement)
  • Overlying skin infection
  • Diabetes Mellitus
  • Arthritic Joints, Prosthetic joints
  • Elderly, Immunocompromised states
  • Recent joint surgery or procedure


Common Organisms
  • Staph Aures 40%
  • Streptocossus 30%
  • GNB 20%
  • Gonococcal arthritis - Most common cause of septic arthritis in the sexually active patient population. Presents as migratory polyarthritis and may involve several joints (wrist, knee and ankles), or include a rash/tenosynovitis. 4:1 female to male predominance.

Clinical Presentation (No combination of exam findings can definitively diagnose septic arthritis)
  • Typical - Swollen, Red, Immobile and Tender joint
  • Pain is present in about 80%. Joint tenderness has sensitivity approaching 100%
  • Fever is seen only in about 50% 
  • Generalized tenderness with painful limitation of active and passive range of motion. Focal tenderness and pain limited to specific movements on an active range of motion testing is more typical of periarticular inflammation (skin, bursa, tendons).
Immunocompromised patients often have polyarticular involvement and present atypically. Sudden onset of pain is more suggestive of intrinsic joint pathology, such as septic arthritis.


Work up (Serum blood tests do not rule out septic arthritis)
  • Synovial Fluid Analysis - Synovial fluid with a WBC count > 50,000/mm with a polymorphonuclear cell count > 90%. However, in culture-proven septic arthritis, this WBC count is reached only in 50 – 75% of casesTherefore, lower WBC counts cannot exclude the presence of septic arthritisA synovial fluid WBC count >100,000/mm is more specific. MRSA-associated septic arthritis (leading cause in prosthetic joints) may have lower synovial fluid WBC counts only up to 15,000 cells/μL
  • Use CRP/ESR/WCC with caution - Normal levels cannot rule out septic arthritis
  • Positive Gram stain can be diagnostic; however, a negative result for bacteria cannot rule out septic arthritis (sensitivity only 50-60%). Culture remains the most sensitive test (>90%).
  • Presence of crystals shouldnot be used to rule out septic arthritis. Gout and Septic Arthritis can co-exist in the same joint. 


Synovial lactate has the best diagnostic accuracy in septic arthritis, based on several studies. Levels above 10 mmol/L demonstrate +LRs ranging from 20 to infinity

Imaging tests offer little assistance in the diagnosis of septic arthritis. Radiographs may demonstrate effusion or soft tissue swelling. Computed tomography (CT) has greater sensitivity for effusions and edema but is unreliable early in the disease course to evaluate for septic arthritis. Ultrasound (US) can be used to localize joint swelling and target the site for optimal aspiration. 


Management
  • Analgesia
  • Joint aspiration
  • Empiric Antibiotics (should provide gram-positive and gram-negative coverage)
  • Orthopedic Referral consultation

Take Home
  • More abnormal joint, more likely Septic Arthritis
  • Immunocompromised patients often have polyarticular involvement and present atypically. 
  • Sudden onset of pain is more suggestive of intrinsic joint pathology, such as septic arthritis.
  • Serum blood tests do not rule out septic arthritis
  • If suspicion is still high after equivocal or dry tap, admit the patient and initiate empiric IV antibiotics while the synovial culture results


Posted by:


              
     Lakshay Chanana
     
     ST4 Trainee
     Royal Infirmary of Edinburgh
     Department of Emergency Medicine
     Edinburgh
     Scotland

     @EMDidactic



Sunday, January 27, 2019

Myths in Diagnosis of ACS

Myth 1
Absence of Classic Chest Pain obviates the need for ACS work up

The absence of chest pain in no way excludes the diagnosis of ACS. Around 33-50% of the patients with ACS present to the hospital without chest pain. Close to 20% of patients diagnosed with acute MI present with symptoms other than chest pain. Risk factors associated with the absence of chest pain included age, female gender, non-white race, diabetes mellitus, and a prior history of congestive heart failure or stroke. Over the age of 85, 60–70% of patients with acute MI present without chest pain; shortness of breath is the most frequent anginal equivalent in this population.

Patients experiencing an acute MI without chest pain are more likely to suffer delays in their care. They were also more likely to die in the hospital compared to patients who presented with chest pain. Over the age of 85, 60–70% of patients with acute MI present without chest pain.


Myth 2
Reproducible chest wall tenderness on palpation rules out ACS
The combination of three variables – sharp or stabbing pain, no history of angina or acute MI, and pain that was pleuritic, positional, or reproducible – is considered as a very low-risk group. Chest pain localized to a small area of the chest is often thought to suggest a musculoskeletal etiology. In one study, however, 27 of 403 patients (7%) with acute MI localized their pain to an area as small as a coin. On examining the patient, one should be careful in determining if the pain induced by chest palpation is the same pain as the presenting pain and more importantly think if the history is congruent with MSK pain. If there is no defined injury or event that could have led to a soft tissue injury, we should be reluctant to render a diagnosis of musculoskeletal pain.


Several studies have shown that chest wall tenderness can be misleadingAlthough certain chest pain characteristics decrease the likelihood of acute MI, none is powerful enough to support discharging at-risk patients without additional testing. In patients with chest pain, chest wall tenderness may suggest that acute MI is less likely but it does not effectively rule out the diagnosis. Given the potential implications of missing ACS, using chest wall tenderness as an independent rule out strategy is not recommended in patients at risk for ACS.



Myth 3
A normal ECG and normal cardiac enzymes rule out ACS
No historical complaint, physical finding, or ECG pattern has a negative predictive value of 100% for MI. Rather the correct statement would be this - Patient is less likely to be experiencing an MI if the ECG is normal, but further work up is needed to discard the diagnosis. Use ECG as more of a rule-in test, not a rule-out test. 

Cardiac markers provide a non-invasive means of determining whether myocardial damage has occurred. When ischemia gives way to infarction, the myocardial cell membrane is disrupted and various chemical markers are released into the systemic circulation. 
Cardiac Troponins  (I or T) are now the preferred cardiac markers for identifying myocardial damage. It is important to remember that troponin can only detect myocardial cell death but not ischemia.


Take Home:
  • Do not exclude the diagnosis of acute cardiac ischemia or MI based on the absence of pain, especially when evaluating dia- betic patients, the elderly, and women.
  • Never use reproducible chest wall tenderness to exclude the diagnosis of acute MI.
  • Neither a single normal ECG nor a single negative set of cardiac enzymes should be used to rule out acute cardiac schema. 


References:


  1. Canto JG, Shlipak MG, Rogers WJ, et al. Prevalence, clinical characteristics, and mortality among patients with myocardial infarction presenting without chest pain. J Am Med Assoc 2000; 283:3223–9.
  2. 2. Dorsch MF, Lawrence RA, Sapsford RJ, et al. Poor prognosis of patients presenting with symptomatic myocardial infarction but without chest pain. Heart 2001; 86:494–8.
  3. Gupta M, Tabas JA, Kohn MA. Presenting complaint among patients with myocardial infarction who present to an urban, public hospital emergency department. Ann Emerg Med 2002; 40:180–6.
  4. Uretsky BF, Farquahr DS, Berezin AF, et al. Symptomatic myocardial infarction without chest pain: prevalence and clini- cal course. Am J Cardiol 1977; 40:498–503.
  5. Bayer AJ, Chadha JS, Farag RR, et al. Changing presentation of myocardial infarction with increasing old age. J Am Geriatr Soc 1986; 34:263–6.
  6. Lee TH, Cook EF, Weisberg MC, et al. Acute chest pain in the emergency room. Identification and examination of low risk patients. Arch Intern Med 1985; 145:85–9.
  7. Lee TH, Rouan GW, Weisberg MC, et al. Clinical characteristics and natural history of patients with acute myocardial infarction sent home from the emergency room. Am J Cardiol 1987; 60:219–24.
  8. Solomon CG, Lee TH, Cook EF, et al. Comparison of clinical presentation of acute myocardial infarction in patients older than 65 years of age to younger patients: the Multicenter Chest Pain Study experience. Am J Cardiol 1989; 63:772–6.
  9. Swap CJ, Nagurney JT. Value and limitations of chest pain his- tory in the evaluation of patients with suspected acute coronary syndromes. J Am Med Assoc 2005; 294:2623–9. 


Posted by:

              
     Lakshay Chanana
     
     ST4 Trainee
     Royal Infirmary of Edinburgh
     Department of Emergency Medicine
     Edinburgh
     Scotland

     @EMDidactic