PoCUS in Pericardial Effusion

Medical Student Clinical Pearl – October 2019

 

Alex Pupek

Faculty of Medicine
Dalhousie University
CC4
Class of 2020

Reviewed and Edited by Dr. David Lewis

 


Case

A 70F with a history of bladder CA, HTN and 4.9cm AAA presented to the Emergency Department (ED) and was Triaged as Level 3 with a chief complaint of generalized weakness. Initial assessment was significant for hypotension and low-grade fever with dysuria elicited on history; she was started on Ceftriaxone with a working diagnosis of urosepsis. Bloodwork and imaging studies were sent to rule out other potential sources of infection.

She had a mild leukocytosis of 12.4, pH of 7.23 and a lactate of 5.0. Point-of-care urinalysis was unremarkable. The chest x-ray revealed an enlarged cardiothoracic ratio of 0.62 compared to 0.46 ten months previously, concerning for a pericardial effusion.

Upon reassessment, the patient appeared unwell with slight mottling to the skin, cool extremities and tenuous blood pressure; point of care ultrasound revealed a large pericardial effusion.  Interventional cardiology was paged; the patient was moved to the trauma area and an emergent pericardiocentesis was performed: 360cc of bloody fluid was removed. The pericardial drain was left in situ.

Post-procedure bloodwork included a troponin of 216 and CK of 204. The patient was admitted to the Cardiac Care Unit and discharged within a week’s time.

 


Pericardial Effusions and The Role of Point-of-Care Ultrasound (POCUS)

The normal pericardial sac contains up to 50 mL of plasma ultrafiltrate [1]. Any disease affecting the pericardium can contribute to the accumulation of fluid beyond 50mL, termed a pericardial effusion. The most commonly identified causes of pericardial effusions include malignancy and infection (Table 1).

 

Table 1 – UpToDate, 2019 – Diagnosis and Treatment of Pericardial Effusions


 

Evaluation of the pericardium with point-of-care ultrasound includes one of four standard views: parasternal long axis, parasternal short axis, subxiphoid and apical (Figure 1). A pericardial effusion appears as an anechoic stripe or accumulation surrounding the heart. Larger effusions may completely surround the heart while smaller fluid collections form only a thin stripe layering out posteriorly with gravity. Seen most commonly post-cardiac surgery, pericardial effusions may be loculated and compress only a portion of the heart. [1,2] (Table 2)

Figure 1[1]


Table 2 [2]


 

Both the pericardial fat pad and pleural effusions can be mistaken for pericardial effusions. The parasternal long-axis view is most helpful to accurately define the effusion with the descending aorta, posterior to the mitral valve and left atrium, serving as a landmark: the posterior pericardial reflection is located anterior to this structure. Fluid anterior to the posterior pericardial wall is pericardial, whereas a pleural effusion will lie posterior. The pericardial fat pad is an isolated dark area with bright speckles, located anteriorly; unlike fluid, it is not gravity dependent. Rather than competing with the cardiac chambers for space within the pericardial sac, the fat pad moves synchronously with the myocardium throughout the cardiac cycle. [1,2] (Figure 2)

Figure 2[1]


A pericardial effusion discovered on POCUS in the ED may be mistaken for tamponade, leading to inappropriate and invasive management in the form of pericardiocentesis.[2]

Patient tolerance of pericardial effusions depends on the rate by which they accumulate. As little as 150-200 mL of rapidly accumulating effusion can cause tamponade whereas much larger amounts of slowly accumulating fluid can be well tolerated. Pericardial effusions formed gradually are accommodated by adaptations in pericardial compliance. A tamponade physiology is reached once the intrapericardial pressure overcomes the pericardial stretch limit.[2] (Figure 3)

Figure 3[2]


The core echocardiographic findings of pericardial tamponade consist of:

  • a pericardial effusion
  • diastolic right ventricular collapse (high specificity)
  • systolic right atrial collapse (earliest sign)
  • a plethoric inferior vena cava with minimal respiratory variation (high sensitivity)
  • exaggerated respiratory cycle changes in mitral and tricuspid valve in-flow velocities as a surrogate for pulsus paradoxus

In the unstable patient with clinical and echocardiographic findings of tamponade, an emergent pericardiocentesis is indicated.[2]

A retrospective cohort study of non-trauma emergency department patients with large pericardial effusions or tamponade, ultimately undergoing pericardiocentesis, found that effusions identified by POCUS in the ED rather than incidentally or by other means saw a decreased time to drainage procedures, (11.3 vs 70.2 hours, p=0.055).[3]

Point of care ultrasound is a valuable tool during the initial evaluation of the undifferentiated hypotensive emergency department patient but should be interpreted judiciously and within clinical context to avoid unnecessary emergency procedures.


Additional Images

From GrepMed


 

echocardiogram-pericardial-tamponade-alternans-effusion

 


References

  1. Goodman, A., Perera, P., Mailhot, T., & Mandavia, D. (2012). The role of bedside ultrasound in the diagnosis of pericardial effusion and cardiac tamponade. Journal of emergencies, trauma, and shock, 5(1), 72.
  2. Alerhand, S., & Carter, J. M. (2019). What echocardiographic findings suggest a pericardial effusion is causing tamponade?. The American journal of emergency medicine, 37(2), 321-326.
  3. Alpert, E. A., Amit, U., Guranda, L., Mahagna, R., Grossman, S. A., & Bentancur, A. (2017). Emergency department point-of-care ultrasonography improves time to pericardiocentesis for clinically significant effusions. Clinical and experimental emergency medicine, 4(3), 128.

 

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Hemiplegic Migraine

Medical Student Clinical Pearl – January 2020

Alyssa BeLong, B.Sc.(Hon)

Dalhousie Medicine New Brunswick

M.D. Candidate, Class of 2021

Reviewed and Edited by Dr. David Lewis


Case Presentation

A 45-year-old female presented with sudden-onset left-sided vision loss, right arm paralysis and auditory changes 24 hours ago. She subsequently developed a throbbing pain (6/10) behind her left eye which radiated over her scalp, with a sensation of water dripping down the back of her neck. Her symptoms resolved within 30 minutes except for ongoing headache and photophobia.


Differential Diagnosis

A variety of conditions may present with transient unilateral weakness or hemiplegia: (4)

  • Hemiplegic Migraine
  • Transient Ischemic Attack (TIA): Typically present with sudden onset of all symptoms rather than progression from one to another. A TIA is also less likely to present with headache, nausea, photophobia, photophobia.
  • Brain Tumor: Typically present as progressive rather than transient neurologic symptoms.
  • Epilepsy with Post-Ictal Paralysis: Would expect paroxysmal symptoms at time of onset or change in level of consciousness as well as post-ictal confusion. Duration of symptoms also makes this unlikely.
  • Stroke-like Migraine Attacks After Radiation Therapy (SMART)
  • Other possible but rare/unlikely diagnoses include headache and neurologic deficits with cerebrospinal fluid lymphocytosis (HaNDL), CNS infection, Sturge-Weber syndrome as well as certain inherited disorders and metabolic disturbances.

Case Continued – History and Physical Exam

Clarification of visual field disturbance revealed a left homonymous hemianopia rather than loss of vision in the left eye. There was no change in speech or facial droop. There were no precipitating events and there were no alleviating or aggravating factors. The patient noted herself to be particularly stressed lately. She was otherwise healthy with a past medical history of migraines without aura many years prior. Family history was negative for thromboembolic events, she was not taking any medications and had no history of smoking or substance use.

On physical exam, the patient appeared well with all vital signs within normal limits. Cranial nerve exam was unremarkable apart from ongoing photophobia in her left eye. There was normal motor, strength, sensation, tone and reflexes bilaterally. There was no evidence of gait disturbance or dysdiadochokinesia.


Migraine Overview

Migraines typically present as severe episodic headaches often accompanied by photophobia, phonophobia and/or nausea, however presence of an aura can yield a variety of presentations. Migraines are currently thought to be neurologic in origin, although the exact pathophysiology remains unknown (2). Migraines were previously thought to be due to vascular changes, with vasodilation causing headache and vasoconstriction causing aura, however this theory is no longer viable (2).

Migraines affect 17% of women and 6% of men, with an overall prevalence of 12% (2). Migraines typically flow through four phases (2):

  1. Prodrome: Change in affect or vegetative symptoms 24-48hrs prior to onset of headache.
  2. Aura: Focal neurologic symptoms, including visual, sensory, language or motor disturbance.
  3. Headache: Often unilateral but can be bilateral, typically throbbing or pulsatile in quality, frequently accompanied by photophobia, phonophobia, nausea or vomiting.
  4. Postdrome: Sudden movement may trigger transient pain in location of the resolved headache.

While many types of migraines exist, 75% of migraines do not have an aura (2). Some patients also experience aura without headache. Factors thought to be involved in precipitation of migraine include stress, menstruation, fasting, weather, nitrates, wine and visual triggers (2, 3).  

Hemiplegic Migraine

  1. At least two attacks fulfilling criteria B and C
  2. Aura consisting of both of the following:
    1. Fully reversible motor weakness
    2. Fully reversible visual, sensory and/or speech/language symptoms
  3. At least two of the following four characteristics:
    1. At least one aura symptom spreads gradually over ≥5 minutes, and/or two or more symptoms occur in succession
    2. Each individual non-motor aura symptom lasts 5 to 60 minutes, and motor symptoms last <72 hours
    3. At least one aura symptom is unilateral
    4. The aura is accompanied, or followed within 60 minutes, by headache
  4. Not better accounted for by another ICHD-3 diagnosis, and transient ischemic attack and stroke have been excluded

Familial hemiplegic migraine requires one first or second degree relative to meet the above criteria for hemiplegic migraine. Sporadic hemiplegic migraine encompasses those who do not meet familial criteria. (4, 5).

  1.  

Treatment

Treatment of acute migraine in the emergency department follows similar principles to abortive management in an outpatient setting (6):

Abortive Agents

  • Triptans
    • Sumatriptan 6mg SC
  • Antiemetics / Dopamine Receptor Blockers
    • Metoclopramide 10mg IV, Prochlorperazine 10mg IV or Chlorpromazine 0.1mg/kg IV up to 25mg IV)
    • Diphenhydramine: given with parenteral antiemetics to prevent akathisia or dystonia. 12.5-25mg IV (q1h up to two doses)
  • Dihydroergotamine 1mg IV + Metoclopramide 10mg IV can be given if Metoclopramide monotherapy is ineffective.
  • Dexamethasone 10-25mg IV (or IM): Recommended in conjunction with the above treatments to lower risk of early headache recurrence.

In general, hemiplegic migraines can be treated the same as typical migraine with aura (4). Triptans and ergotamine are currently contraindicated due to their effect on vasoconstriction and theoretical risk of ischemic events, although this recommendation may change with evolving theory of migraine pathophysiology (4, 7).

Opioids are not recommended as first-line therapy and should not be routinely used in the acute management of migraine (6, 8).  


Case Continued – Treatment

The following medications were given in the emergency department:

  1. 10mg Metoclopramide IV
  2. 1mg Benztropine IV (for prevention of dystonia)
  3. 10mg Dexamethasone IV

Case Conclusion

The patient’s headache resolved with IV medications. She was advised to take it easy and consider scaling back on her shifts at work – a significant source of her stress. The patient was very pleased with her treatment and was discharged home.


Sources

  1. Donnelly K (2011). Homonymous Hemianopsia. In: Kreutzer J.S., DeLuca J., Caplan B. (eds) Encyclopedia of Clinical Neuropsychology. Springer, New York, NY. DOI: https://doi.org/10.1007/978-0-387-79948-3_739
  2. Cutrer F. Pathophysiology, clinical manifestations, and diagnosis of migraine in adults. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on December 23rd, 2019.)
  3. Martin VT, Behbehani MM (2001). Toward a rational understanding of migraine trigger factors. Medical Clinics of North America 85(4):911.
  4. Robertson C. Hemiplegic Migraine. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on December 23rd, 2019.)
  5. Headache Classification Committee of the International Headache Society (IHS) (2013). The International Classification of Headache Disorders, 3rd edition (beta version). Cephalalgia 33(9):629-808. DOI: 10.1177/0333102413485658
  6. Smith J. Acute Treatment of Migraine in Adults. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on December 23rd, 2019.)
  7. Russell MB, Ducros A (2011). Sporadic and familial hemiplegic migraine: pathophysiological mechanisms, clinical characteristics, diagnosis, and management. Lancet Neurology 10(5):457-70. DOI: 10.1016/S1474-4422(11)70048-5
  8. Friedman BW, West J, Vinson DR, Minen MT, Restivo A, Gallagher EJ (2015). Current management of migraine in US emergency departments: an analysis of the National Hospital Ambulatory Medical Care Survey. Cephalalgia 35(4):301.
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Tardive Dyskinesia in an Emergency Setting

Medical Student Clinical Pearl – October 2019

Faith Moore

Faculty of Medicine
Dalhousie University
CC3
Class of 2021

Reviewed and Edited by Dr. David Lewis



Case

A 48-year-old female was brought to the emergency department by EMS after developing dystonia that morning, a couple hours earlier, following a restless night. The dystonia had begun affecting her arms, torso and buccal region, but eventually moved to also involve her legs. She had a history of recurrent tardive dyskinesia for the past 20 years since taking stelazine and developing tardive dystonia. She was switched to olanzopine after developing dystonia and stayed on it until two months ago. Her citalopram and clozapam dosing had been increased two weeks ago, and she had also started Gingko biloba extract two weeks ago. She had started Nuplazid 3 days ago.

Upon exam she was diaphoretic with no other abnormal findings other than dystonia affecting the entire body.


Tardive Dyskinesia

Pathophysiology

    • Tardive dyskinesia is a hyperkinetic movement disorder that is associated with the use of dopamine receptor-blocking medications.1 The exact mechanism is under debate, but the main hypotheses include an exaggerated response by dopamine receptors due to a chronic dopamine blockade, oxidative stress, gamma-aminobutyric acid (GABA) depletion, cholinergic deficiency, altered synaptic plasticity, neurotoxicity and defective neuroadaptive signaling. 2 The most accepted theory of the mechanism is that the chronic dopamine blockade caused by the dopamine receptor-blocking medications results in a hypersensitivity of the receptors, specifically at the basal ganglia. 1
    • The medications that are known to have the possibility to cause tardive dyskinesia include antipsychotic drugs, anticholinergic agents (ex. Procyclidine), antidepressants, antiemetics (ex. Metoclopramide), anticonvulsants, antihistamines, decongestants (ex. pseudoephedrine and phenylephrine), antimalarials, antiparkinson agents, anxiolytics, biogenic amines, mood stabilizers and stimulants.1

Who is most at risk?

    • The medications that are the most common culprits are first- and second-generation antipsychotics and metoclopramide. The incidence of tardive dyskinesia from chronic first-generation antipsychotic exposure is 5-6% 3, and is 4% for second generation antipsychotics 4. There is no prospective research on chronic metoclopramide use and the risk for tardive dyskinesia at this point and time5, but a study in the UK in 1985 showed 1 case of tardive dyskinesia for every 35 000 prescriptions6.
      • Most prominent risk factors
        • Old age5
        • Chronic exposure5
        • Patients who develop extrapyramidal symptoms while on antipsychotic drugs.7

Signs and Symptoms

      • Repetitive involuntary body movements that may involve the face, tongue, eyes, arms, torso and legs

Diagnosis

    • The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) classifies tardive dyskinesia as “involuntary movements (lasting at least a few weeks) generally of the tongue, lower face and jaw, and extremities (but sometimes involving the pharyngeal, diaphragmatic, or trunk muscles), developing in association with the use of a neuroleptic medication for at least a few months” and that persists for at least one month after the medication is stopped.8

Differential Diagnosis

    • Acute dyskinesia
    • Akathisia
    • Parkinsonism and tremor
    • Perioral tremor
    • Stereotypies and mannerisms
    • Spontaneous or idiopathic dyskinesias
    • Isolated dystonia
    • Primary movement disorders
    • Chorea from systemic causes 9

Key Questions for History and Physical

    • Are the movements voluntary?
    • Is there an accompanied feeling of restlessness?
      • If yes, might point towards akathisia.
    • When did these movements began?
    • What is the body distribution of the involuntary movements?
    • Are there any extrapyramidal signs and symptoms?
    • Are there any associated features?
    • Have there been any drug changes in the past few months?

 

Management in the Emergency Department

    • First line treatment of tardive dyskinesia generally begins with discontinuation of the offending drug. In the emergency department this should be done after consulting with the treating physician. These patients are often being treated for psychiatric disorder and the treatment of the psychiatric disorder must be balanced with the risk of tardive dyskinesia. It may be appropriate to switch from a first generation antipsychotic medication to a second generation antipsychotic generation medication.
    • If the symptoms of tardive dyskinesia need to be treated, like in our case with this patient, there are various drugs that can be tried.
    • Tetrabenazine is considered first line.10
      • Suggested doses of 12.5-25 mg starting daily dose with a 25-200 mg/day dose range.10
    • Other treatment options
      • Dextromethorphan11
        • In a recent case study patients took under 1mg/kg, not exceeding 42 mg/day.11
        • This was recommended by a local neurologist here at the Saint John Regional Hospital.
      • Valbenazine 12
        • Suggested dose of 40 mg UID, increasing to 80 mg UID after one week.12
      • Amantadine10
        • Suggested dose of 100 mg starting daily dose with a dose range of 100-300 mg/day 10
      • Benzodiazepines12
        • Clonazepam initiated at 0.5 mg and titrated by 0.5 mg increments every 5 days to response up to a maximum dose of 3-4 mg/day. 12
      • Diphenhydramine suggested dose of 25-50 mg IV13
      • Botulinum toxin injections12
    • Commonly used treatments lacking evidence of efficacy
      • Benztropine10

Drug Starting Dose Recommendations Dose Range
1st Line
Tetrabenazine 12.5-25 mg UID 25-200 mg UID
Other options
Dextromethorphan Under 1 mg/kg Not exceeding 42 mg UID
Valbenazine 40 mg UID Increase to 80 mg after 1 week
Amantadine 100 mg UID 100-300 mg UID
Clonazepam 0.5 mg 0.5-4.0 mg UID
Diphenhydramine 25 mg IV 25-50 mg IV
Botulinum toxin injection local injection to treat specific painful dystonia resistant to systemic therapy

 


Case Continued

The patient was given 2mg of Benztropine IV with no effect. Twenty minutes later he was then given 1mg of Ativan SL with no effect. Thirty minutes later the patient was given 150 mg Benadryl IV, and some improvement was then witnessed, the patient was allowed to sleep and was discharged approximately 5 hours after his arrival with no symptoms.


External Resources

Treatment strategies for dystonia

Diagnosis & Treatment of Dystonia


References

  1. Cornett EM, Novitch M, Kaye AD, Kata V, Kaye AM. Medication-Induced Tardive Dyskinesia: A Review and Update.Ochsner J. 2017 Summer;17(2):162-174. Review. PubMed PMID: 28638290; PubMed Central PMCID: PMC5472076.
  2. Kulkarni SK, Naidu PS. Pathophysiology and drug therapy of tardive dyskinesia: current concepts and future perspectives.Drugs Today (Barc). 2003 Jan;39(1):19-49. Review. PubMed PMID: 12669107.
  3. Glazer WM.Review of incidence studies of tardive dyskinesia associated with typical antipsychotics. J Clin Psychiatry. 2000;61 Suppl 4:15-20.  PubMed PMID: 10739326.
  4. Correll CU, Schenk EM.Tardive dyskinesia and new antipsychotics. Curr Opin Psychiatry. 2008 Mar;21(2):151-6. doi: 10.1097/YCO.0b013e3282f53132.  PubMed PMID: 18332662.
  5. Rao AS, Camilleri M.Review article: metoclopramide and tardive dyskinesia.Aliment Pharmacol Ther. 2010 Jan;31(1):11-9. doi: 10.1111/j.1365-2036.2009.04189.x.  PubMed PMID: 19886950.
  6. Bateman DN, Rawlins MD, Simpson JM.Extrapyramidal reactions with metoclopramide. Br Med J (Clin Res Ed). 1985 Oct 5;291(6500):930-2. doi: 10.1136/bmj.291.6500.930. PubMed PMID: 3929968; PubMed Central PMCID: PMC1417247
  7. Novick D, Haro JM, Bertsch J, Haddad PM.Incidence of extrapyramidal symptoms and tardive dyskinesia in schizophrenia: thirty-six-month results from the European schizophrenia outpatient health outcomes study. J Clin Psychopharmacol. 2010 Oct;30(5):531-40. doi: 10.1097/JCP.0b013e3181f14098. PubMed PMID: 20814320.
  1. American Psychiatric Association, Medication-induced movement disorders and other adverse effects of medication, Diagnostic and Statistical Manual of Mental Disorders, fifth edition, American Psychiatric Association, 2013.
  2. Tarsy D, Deik A. Tardive dyskinesia: Etiology, risk factors, clinical features, and diagnosis. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on September 9, 2019.)
  1. DynaMed [Internet]. Ipswich (MA): EBSCO Information Services. 1995 – . Record No.T113751, Tardive Dyskinesia; [updated 2018 Nov 30, cited September 9, 2019]. Available from https://www.dynamed.com/topics/dmp~AN~T113751. Registration and login required.
  1. Kim J. (2014). Dextromethorphan for Tardive Dyskinesia. International Neuropsychiatric Disease Journal. 2. 136-140. 10.9734/INDJ/2014/7970.
  2. Tarsy D, Deik A. Tardive dyskinesia: Prevention, prognosis, and treatment. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on September 9, 2019.)
  1. Buttaravoli P, Leffler SM. Chapter 1 – dystonic drug reaction. 2012:1-3. doi:https://doi.org/10.1016/B978-0-323-07909-9.00001-5 “.
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Palpitations – A Paroxysmal Pearl

Palpitations – A Paroxysmal Pearl

Medical Student Clinical Pearl

Scott Fenwick

Class of 2021

Faculty of Medicine
Dalhousie University

Reviewed and Edited by Dr. David Lewis


Case Presentation:

A 49-year-old female presented with palpitations for the past 2 hours. She had two similar episodes in the last 2 weeks, both of which resolved within 1-2 minutes. She had no other symptoms. She was otherwise healthy, with no past medical history. She was a non-smoke and non-drinker who leads an active lifestyle. She denied weight loss, diarrhea, and heat intolerance.

On physical exam, she was tachycardic at 130bpm with an irregularly irregular pulse. She did not display any tremor or diaphoresis. On auscultation, S1 and S2 were audible, with no murmurs or extra sounds. Respiratory and abdominal exams were unremarkable.


What to ask on History?

Common Symptoms: palpitations, tachycardia, fatigue, weakness, dizziness, light-headedness, reduced exercise capacity, mild dyspnea, and polyuria. It is essential to know when exactly the symptoms started. AF that presents before 48 hours can be safely rhythm controlled without anticoagulation.(1)

Severe/Secondary Symptoms: angina, dyspnea at rest, presyncope and, uncommonly, syncope. Embolic events and heart failure can be severe complications of AF.

Past Medical History: cardiovascular or cerebrovascular disease, diabetes, hypertension, COPD, obstructive sleep apnea, and hyperthyroidism.


What to look for On Examination?

ABCs and vitals: particularly pulse rate and rhythm.

General Assessment: look for signs of thyroid disease, PE, pulmonary disease, alcohol withdrawal, and signs of liver disease from excessive alcohol ingestion.

CVS: precordial scars from prior cardiac surgery, JVP, peripheral edema, and auscultation for murmurs or additional sounds that might suggest valvular AF. There is often an apical-radial pulse deficit where not every apical beat has an associated radial beat due to lack of left ventricular stroke volume.(2)


Case Continued – Testing:

The patient was put on a cardiac monitor and an ECG was performed, demonstrating atrial fibrillation. There was also a right bundle branch block that was consistent with a previous ECG performed in 2017. Laboratory testing was unremarkable.

Depending on clinical suspicion, initial testing may include CBC, electrolytes, blood glucose, PT/INR, creatinine, BUN, TSH, cardiac enzymes, LFTs, and chest x-ray.2

See Basic ECG interpretation Pearl for a great guide to ECGs

Basic ECG Interpretation


 

Classifying Atrial Fibrillation:

AF is classically described as an irregularly irregular heartbeat, as can be observed from the variable RR intervals in the ECG above. In AF, there are no distinct P-waves due to the uncoordinated atrial activity. Broadly, AF can be divided into valvular and non-valvular subtypes. Non-valvular AF can be classified into the following categories:(1)

  • Paroxysmal – AF terminates spontaneously or with intervention within 7 days of onset.
  • Persistent – AF fails to terminate within 7 days of onset; often a progressive disease.
  • Long-Standing Persistent – AF has persisted for greater than 12 months.
  • Permanent – Joint decision between patient and provider to no longer pursue rhythm control.

AF commonly progresses from paroxysmal to persistent states. The above classification only refers to primary atrial fibrillation, not AF that is secondary to cardiac surgery, pericarditis, myocardial infarction, valvulopathy, hyperthyroidism, pulmonary embolism, pulmonary disease, or other reversible causes.

For persistent and permanent AF, the CHADS2 score can be used to estimate a patient’s 1-year risk of ischemic stroke without anticoagulation (0 = low risk, 1-2 = moderate risk, 3+ = high risk).(1)

Calculate it here

 

CAEP and CCS now recommend using the CHAD-65 Score to determine anticoagulation requirement.

 


 

Treatment

DC and chemical (e.g. procainamide) cardioversion are two well-described methods of treating uncomplicated AF. The goal of treatment is to return patients to NSR. Some important points about the two methods include:

  • DC cardioversion can be administered at an initial energy dose of 100J and increased up to 360J as needed.(2)
  • Procainamide is often given in doses of 15-18mg/kg, or more simply, 1g over 60 minutes. Average time to cardioversion is about 1 hour.(1)
  • DC cardioversion requires procedural sedation; whereas, chemical cardioversion does not.
  • In a recent RCT, combination therapy achieved NSR in 99% of patients; Attempting DC cardioversion first decreased length of hospital stay by 1.2 hours.(3)
  • Both therapies are generally well-tolerated by patients.

Case Continued – Treatment:

The patient was diagnosed with paroxysmal atrial fibrillation. The arrhythmia did not spontaneously resolve in the ED. DC and chemical cardioversion methods were considered and discussed with the patient. Direct Current (DC) cardioversion was performed under procedural sedation with propofol and fentanyl. Shocks of 100J and 200J were unsuccessful in converting the patient into normal sinus rhythm (NSR). A third shock at 300J was ultimately successful. The following ECG was obtained demonstrating NSR. As in the initial ECG, there is a RBBB present.

 

CHADS2 score was 0. Therefore anticoagulation or antithrombotic therapy not indicated.


 

Case Conclusion:

The patient was discharged home within 4 hours of arriving to hospital, anticoagulation was not prescribed. It is likely that she will experience AF again and require anticoagulation later in life.


 

References:

  1. January, C. T., Wann, L. S., Alpert, J. S., Calkins, H., Cigarroa, J. E., Cleveland, J. C., et al. (2014). 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: Executive summary. Journal of the American College of Cardiology, 64(21), 2246. doi:10.1016/j.jacc.2014.03.021
  2. Wakai, A., & Neill, J.O. (2003). Emergency management of atrial fibrillation. Postgrad Med J, 79(932), 313. doi:10.1136/pmj.79.932.313
  3. Scheuermeyer, F. X., Andolfatto, G., Christenson, J., Villa-Roel, C., & Rowe, B. (2019). A multicenter randomized trial to evaluate a chemical-first or electrical-first cardioversion strategy for patients with uncomplicated acute atrial fibrillation. Academic Emergency Medicine, 26(9), 969-981. doi:10.1111/acem.13669
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Approach to Resuscitation in Severe Calcium Channel Blocker Poisoning

Medical Student Clinical Pearl

J.L. Dobson

Faculty of Medicine
Memorial University of Newfoundland
M.D. Candidate 2020

Reviewed and Edited by Dr. Luke Taylor and Dr. David Lewis

and Liam Walsh. Pharmacist HHN


 

Introduction:

Calcium channel blockers (CCBs) have multiple clinical uses, including the management of hypertension, angina, and cardiac arrhythmias. [1] While CCBs are no longer the most widely prescribed antihypertensive as they were in the 1990s, their prevalence remains high. [2] This along with the existence of both immediate release and long-acting forms poses a challenge for the Emergency Physician faced with a case of CCB poisoning.

Physiology:

Myocardium in the sinoatrial and atrioventricular nodes uses the slow action potential created by calcium currents to conduct. CCBs act on this tissue by inhibiting this current, thus slowing conduction through the SA and AV nodes. This results in a decreased heart rate, prolonged PR intervals, and lengthened refractory periods through the AV node. Conversely, they also inhibit calcium flow in smooth muscle, resulting in coronary and peripheral artery dilation. This ultimately provides the mechanism for reflex tachycardia, increased AV conduction, and improved myocardial contractility. [3]

Adverse reactions to the physiological effects of CCBs include vasodilatory effects (peripheral edema, headache, palpitations), gastrointestinal effects (nausea, diarrhea, constipation), and negative inotropic effects (hypotension, bradycardia). [4]


 

Case Report:

A 80-year-old male is brought in to Trauma by ambulance with hypotension, bradycardia, and an altered level of consciousness. Report from EMS reveals the patient called about half an hour prior stating that he had taken medications in an attempt to commit suicide. Upon arrival, the pt was alert and oriented, and endorsed taking an unknown quantity of clonazepam and citalopram, and a deficit of up to four grams of Diltiazem was noted from his medications. He denied further substance use. Though initially stable, the patient deteriorated rapidly upon arrival to the emergency department.

In the Emergency Department, initial vitals revealed a BP of 88/68, P of 52 bpm and SPO2 of 93% on RA and a BG of 15. As such nasal prongs were placed and she was immediately given atropine as well as push dose epinephrine. Within ten minutes, there was further decline in mental status of the patient corresponding to a blood pressure of 83/61 and a heart rate persisting in the low 40s bpm. He was successively given further epinephrine, atropine and calcium chloride while toxicology was contacted. Despite recurrent doses of epinephrine and atropine, the patient remained profoundly hypotensive and bradycardic. Insulin (Humulin R) and dextrose were started at 0.5U/kg/hr with a 1U/kg bolus. This infusion was titrated up every thirty minutes with minimal improvement in vitals. At this point, remaining bradycardic at 37bpm, intralipid therapy was deemed necessary and so a bolus of 105mL was given. Having received epinephrine bolus along with a 0.2mcg/kg/hr infusion, maximum dose of atropine, 3g of Calcium chloride, with minimal clinical improvement cardiac pacing was initiated. Once good electrical and mechanical capture were achieved the patient underwent and RSI with ketamine and rocuronium. Once stabilized, he was transferred to ICU for further management. In ICU, the patient had a transvenous pacemaker floated successfully followed by a transitioning off the epinephrine to norepinephrine and vasopressin. Intralipid infusion was started and the insulin and glucose therapy was titrated up to a maximum of 4U/kg/hr. The patient unfortunately did not tolerate whole bowel irrigation. Despite the critical nature of their condition, the patient did slowly improve and pressors were weaned.


 

Discussion:

History & Primary Survey

This patient experienced negative inotropic effects of the extended release calcium channel blocker, resulting in cardiogenic shock. Ingestion of more than 5-10 times the usual dose of CCB results in severe intoxication: this patient was thought to have consumed four grams of Diltiazem, over eleven times the maximum recommended dose. [5] While any CCB can result in hypotension, knowledge of which CCB was taken is useful to set expectations for the patient’s progression: unlike dihydropyridine-type CCBs which would more likely present with reflex tachycardia, non-dihydropyridine CCBs like verapamil and diltiazem result in bradycardia. [6] Another crucial point in the primary survey is that, due to the neuroprotective effects of CCBs, mental status may initially be preserved until cerebral perfusion is severely affected. [5]

Initial Resuscitation

While the patient may initially be able to maintain their airway, mental status and vitals may deteriorate rapidly. [5] It is important to note that like any critical ill patient,  intubation may result in a further drop in heart rate and blood pressure via vagal stimulation. It is crucial to have adequate resuscitation prior to intubation. IV crystalloid fluids , IV atropine (up to three 1mg doses), as well as push dose epinephrine are interventions that can be used quickly at bedside to maintain circulation and heart rate while further investigations and treatments can be organized. [5,8]


Specific Treatments

For a severe CCB poisoning in which hypotension is refractory to IV fluids and atropine, all of the following treatments should be administered simultaneously. If the severity is milder, these treatments should be approached in a stepwise fashion, progressing to the next if the preceding treatment is ineffective. [5]

IV Calcium salt:

As a first line recommendation, a calcium chloride bolus (10-20mL 10%) followed by a continuous infusion (0.5 mEq Ca2+/kg/hr) or the equivalent of calcium gluconate is recommended, though often ineffective. [5] Mortality has been shown to be reduced with its administration, and hypercalcemia occurs only rarely. [7] [8]

IV Insulin with dextrose:

High-dose insulin therapy (1 u/kg bolus and 0.5 u/kg/hr infusion up to 10 u/kg/hr) has been shown to be safe and effective at improving hemodynamics, though response is delayed for 30-60 minutes. [5,7] It should be used with calcium and a vasopressor in the presence of myocardial dysfunction. [8] Blood glucose levels should be monitored every 15-30 minutes for hypoglycemia, and 50mL boluses of dextrose (D50W) given accordingly to maintain levels above 8.25 mM. [5] Hypokalemia is another risk of insulin therapy, therefore electrolytes should be monitored every 30 minutes and 20 mEq of potassium chloride given if needed. [5,7]

IV Vasopressor:

Administration of IV epinephrine has shown improvement in cardiac output. [7,8] In the setting of severe CCB poisoning, doses as high as 150mcg per minute of epinephrine may be needed. It is suggested to start the infusion at 2mcg per minute and titrate up to a systolic blood pressure of 100 mmHg, or a MAP of 65 mmHg. [5] These higher doses may result in a large improvement in patient MAP with minimal change in heart rate.

IV Lipid emulsion therapy:

If the patient is refractory to first-line treatments above, or upon consultation with medical toxicology centre, IV lipid emulsion therapy may be recommended. [8] Most commonly, this is given as a bolus of 1.5 mL/kg of 20% lipid emulsion, repeated up to every three minutes for three total boluses. An infusion of 0.25-0.5 mL/kg/minute may be started. [5] Complications of this treatment are still being studied.

Other considerations:

Studies most often show improvement of hemodynamics and no adverse effects with temporary cardiac pacing for bradycardia refractory to first-line treatments. [7,8] Extracorporeal membrane oxygenation may also be necessary if the patient is near cardiac arrest and remains refractory to previous treatments. [8] Dialysis provides no benefit. [5]

Decontamination:

If the patient is asymptomatic and/or hemodynamically stable, 50g of activated charcoal should be given. In the case of ingestion of extended-release CCBs, whole bowel irrigation should be performed regardless of the presence of symptoms. An asymptomatic patient should be monitored for 6-8 hours for immediate release and 24 hours for extended release forms. [5,8]

Investigations:

ECG may reveal PR interval prolongation due to CCB actions on the SA and AV nodes. Frequent blood glucose measurements are crucial to monitor for the effects of insulin treatment and the need for glucose replacement. Serum electrolytes, notably potassium levels, must be assessed for developed hypokalemia secondary to insulin treatment.



Conclusion:

We present a case and review the physiology of a severe calcium channel blocker poisoning. Key considerations in managing a CCB poisoning include specific dosage and form, initial resuscitation with a low threshold for intubation, fluids, and atropine. Further treatments will be required based on severity, such as intravenous calcium, insulin with dextrose, and lipid emulsion therapy, all of which should be initiated promptly if there is concern for massive over dose and patient declining. Other considerations include the need for further vasopressors and temporary cardiac pacing.

 


FIGURE: Society of Critical Care Medicine key recommendations for management of CCB poisoning. Source: “Experts consensus recommendations for the management of calcium channel blocker poisoning in adults.” Crit Care Med. 2017;45(3):e306-e315. DOI: 10.1097/CCM.0000000000002087


 

References:

[1] Elliott, WJ & Ram,CV. J Clin Hypertens (Greenwich). 2011;13:687–689.

[2] Eisenberg, MJ; Brox, A. & Bestawros, AN. Am J Med. 2004;116(1):35-42.

[3] Singh, BN; Hecht, HS; Nademanee, K. & Chew, CYC. Progress in Cardiovascular Diseases. 1982;15(2):103-132.

[4] Russell, RP. Hypertension. 1988;11(3):II42-44.

[5] Barrueto, F. “Calcium channel blocker poisoning.” UpToDate. 2019.

[6] Hofer, CA; Smith, JL & Tenholder, MF. Am J Med. 1993;95(4):431.

[7] St-Onge, M; Dubé, PA; Gosselin, S; Guimont, C; Godwin, J; Archambault, PM; Chauny, JM; Frenette, AJ; Darveau, M; Le Sage, N; Poitras, J; Provencher, J; Juurlink, DN & Blais, R. Clin Toxicol (Phila). 2014;52(9):926.

[8] St-Onge, M; Anseeuw, K; Cantrell, FL; Gilchrist, IC; Hantson, P; Bailey, B; Lavergne, V; Gosselin, S; Kerns, W; Laliberté, M; Lavonas, EJ; Juurlink, DN; Muscedere, J; Yang, CC; Sinuff, T; Rieder, M & Mégarbane, B. “Experts consensus recommendations for the management of calcium channel blocker poisoning in adults.” Crit Care Med. 2017;45(3):e306-e315.

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A focus on PoCUS – A reflection on the value of a PoCUS elective as a medical student

Medical Student PoCUS Elective Reflection

Nick Sajko

Class 2019 Dalhousie Medicine

@saj_ko

 

Nick Sajko, reflects on his experience after completing the SJRHEM PoCUS Elective. Nick is now a PGY1 in Emergency Medicine at the University of Alberta.


 

When my fourth and final year of medical school came around, I was at a crossroads: What did I want to do for the rest of my life? As many will attest, this question influences the choices you make in your clerkship years, especially in deciding on fourth year electives. I was ironically unfortunate in the fact that I had a broad range of interests in a system that does not always benefit those in my situation. I chose electives in Emergency Medicine, Internal Medicine, and Family Medicine – all of them providing valuable learning opportunities and a chance to hone my skills as a junior clinician. However, these “classic” or “bread and butter” electives paled in comparison to the experiences I obtained through my Point of Care Ultrasound (PoCUS) elective at SJRH – a unique elective opportunity relevant to any medical trainee.

 

It is my hope that this reflection piece will provide insight into those deciding on their elective choices and convince some of you to choose a few electives that are off the beat and path and unique. In particular, an elective in the field of PoCUS – a tool that is more useful than some may consider.

 


 

What does a PoCUS elective at SJRH entail? What can I expect?

 

My elective consisted of regularly scheduled shifts within the Emergency Department, paired with senior staff who have specialized training in PoCUS. During these shifts, I would see patients as if I was conducting a bread and butter Emergency Medicine elective, however, cases would be chosen based on the potential for ultrasound practice. This allowed me to gain a remarkable appreciation for the breadth of PoCUS applications within the primary care setting, while also allowing me to gain extremely valuable hands on time with ultrasound in a supervised setting.

 

In addition to the above, I was provided with numerous resources so as to allow for self-directed learning. One of the most valuable resources provided was the opportunity to use the SJRH EM state-of-the-art PoCUS simulator – an invaluable tool for any level of PoCUS experience. Closer to the end of this elective experience, I was offered opportunities to write PoCUS focused case-reports, as well as undergo PoCUS competency exams to solidify my skills within this setting.

The skills I learned in this elective carried forward with me into my various other electives, and provided me with a unique skill-set as a junior learner. Whether it was doing point of care ECHO in my cardiology elective, FAST scans during trauma-codes in my other Emergency Medicine electives, or assessing volume status in complex general internal medicine patients, my competency in these PoCUS applications definitely impressed both residents and staff alike during my fourth year!

 


Why is PoCUS relevant to me as a medical student wanting to specialize in: (insert hyper-specific / niche specialty here)

One question many people may have at this point is, “why would I do this if I wasn’t interested in Emergency Medicine?”. PoCUS is a constantly evolving field, with new and innovative applications being seen in clinical practice constantly. With this, PoCUS can play a huge role in many different specialties: Internal Medicine physicians use PoCUS to provide support to presumed diagnoses and perform certain procedures (such as placing central lines), while surgeons can utilize PoCUS in the examination of traumas, as well as to support diagnoses in the pre- and post-operative patient. PoCUS is steadily becoming a sought after skill in most of the medical and surgical specialties, where proficiency in its use and interpretation can set you apart from other trainees, and more importantly, add to the competency of your patient care!

The value of having this elective through the Emergency Department allows for students to test their skills in the undifferentiated patient – something that will provide learners with enhanced deduction and reasoning skills, no matter what specialty they are interested in. It also allows learners to have access to a huge pool of patients, with a wide breadth of medical problems, thus optimizing this unique elective’s value.

 


 

Is choosing a “unique”, “niche”, or “extra-focused” elective, such as PoCUS, detrimental to my CaRMS application?

Fourth year electives and CaRMS amalgamate into a cruel and unusual game – while most medical school staff and administrators will tell you that your fourth year electives are to be used to “try new things”, this is often not the reality. With the competitiveness of specialties on a constant upward trend, more and more learners choose to conduct the majority of their electives in the single specialty they are interested in. This is great for those who are certain about the field they want to practice in, but creates a predicament for those of us who want to explore a number of options before making a decision.

As I mentioned above, I was in the latter group – with interests spanning 3 different specialties, including some very competitive ones. I chose to go against the grain, so to speak, and opted to conduct a variety of electives in different specialties – including some niche electives in things such as PoCUS. Not only were these opportunities fantastic from a learning point of view, I would argue that they allowed me to stand out amongst a sea of similar applicants and provided me with a unique skill set – something that I think most programs will find enticing! But most importantly, they were fun, exciting, and allowed me to experience my fourth year of medical school the way its advertised.

For those that know their specialty of choice, I would provide the same advice – use this year to experience new things and create a unique learning identity that will set you apart from the rest.

 


 

After all the worry and panic with my elective choices, feeling like I wasn’t committed enough to one specific specialty, I ended up matching to my first-choice field and location. I think this is in large part due to the fact that I was well-rounded in my experiences and had taken the chance to explore unique learning opportunities through this fantastic elective at SJRH. The staff, the environment, and the resources that come with the PoCUS elective at SJRH EM are second to none – I am confident in saying that this elective was the most beneficial and enjoyable component to my fourth year training. Hopefully my thoughts and reflections on this experience will allow some of you to follow a similar path.

 

Nicholas Sajko, B.Sc, MD

Emergency Medicine PGY1

University of Alberta

 


 

Click here for more information on the SJRHEM PoCUS Electives and Fellowships

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PoCUS – Dilated Aortic Root

Medical Student Clinical Pearl

James Kiberd

Class 2019 Dalhousie Medicine

Reviewed and Edited by Dr. David Lewis


Case:

A 66 year-old female presented to the Emergency Department with shortness of breath and back pain. She had a known dilated aortic root, which was being followed with repeat CT scans. Given the nature of her presenting complaint, a PoCUS was performed to assess her aorta.

 

 

 

Long Axis Parasternal View:

PoCUS for Cardiac imaging has been studied in the acute care setting; focusing on the assessment for pericardial effusion, chamber size, global cardiac function, and volume status, and cardiac arrest.1

In the setting of acute aortic dissection, further evaluation is often recommended depending on the practitioner’s skill level.2 There have been case reports where ultrasound has been used to assess both Type A and Type B aortic dissections.3–5

In order to assess the aortic root, have the patient in a supine position. Either the phased array or the curvilinear probe can be used depending on examiner’s preference. The probe should be positioned with the marker towards the patient’s right shoulder on the anterior chest to the left of the patient’s lower left sternal border. By tilting the transducer between the left shoulder and right hip, long axis views are obtained at different levels with the goal of identifying four main structures; the aorta, the left atrium, and the right and left ventricles. The parasternal long axis view of our patient is shown in Figure 1, where her aortic root measured 3.83cm.

 

Figure 1: Parasternal Long Axis View of Heart: Patient’s root diameter was found to be 3.83cm.

More generally, this view can be used to assess left ventricular contractility and the presence of pericardial effusion, which were not present in this patient. She went on to have a confirmatory CT scan where her aortic root was found to be unchanged from her last scan and was 3.8 cm in diameter as assessed by PoCUS.

In Summary:

Although not rigorously studied to assess aortic root dilatation at the bedside, we present a case where PoCUS was reliable in the assessment of the aortic root. There have been other cases of aortic dissection identified by ultrasound in the emergency department setting, however confirmatory studies (either CT scan or formal echocardiography) are still recommended.


References:

  1. Labovitz AJ, Noble VE, Bierig M, et al. Focused cardiac ultrasound in the emergent setting: A consensus statement of the American society of Echocardiography and American College of Emergency Physicians. J Am Soc Echocardiogr. 2010;23(12):1225-1230. doi:10.1016/j.echo.2010.10.005.
  2. Andrus P, Dean A. Focused cardiac ultrasound. Glob Heart. 2013;8(4):299-303. doi:10.1016/j.gheart.2013.12.003.
  3. Perkins AM, Liteplo A, Noble VE. Ultrasound Diagnosis of Type A Aortic Dissection. J Emerg Med. 2010;38(4):490-493. doi:10.1016/j.jemermed.2008.05.013.
  4. Bernett J, Strony R. Diagnosing acute aortic dissection with aneurysmal degeneration with point of care ultrasound. Am J Emerg Med. 2017;35(9):1384.e3-1384.e4. doi:10.1016/j.ajem.2017.05.052.
  5. Kaban J, Raio C. Emergency department diagnosis of aortic dissection by bedside transabdominal ultrasound. Acad Emerg Med. 2009;16(8):809-810. doi:10.1111/j.1553-2712.2009.00448.x.
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PoCUS – Pleural Effusion

Medical Student Clinical Pearl

James Kiberd

Class 2019 Dalhousie Medicine

Reviewed and Edited by Dr. David Lewis


Case: 

A 90 year-old male presented with worsening shortness of breath on exertion, crackles bilaterally at the bases on auscultation with known history of congestive heart failure. Bedside ultrasound was performed to assess for pleural effusion

Lung Views:

In order to perform ultrasound of the lungs, there are four views that are obtained (see Figure 1). Place the patient supine. The high frequency linear array transducer is often used, but either the phased array or curvilinear transducers can be used. The first views are taken at both right and left mid-clavicular lines of the anterior chest. With the marker of the transducer pointed toward the patient’s head, a minimum of 3-4 rib spaces should be identified. The next views are of the posterior-lateral chest. The patient can be supine or in the sitting position. It is these views where a pleural effusion can be identified.

Figure 1: Chest views with ultrasound. ‘A’ are anterior chest view positions and ‘B’ are posterolateral view positions

Pleural Effusion

Pleural effusion is assessed by ultrasound placing the transducer in the midaxillary line with the marker oriented toward the patient’s head. On the patient’s right side the diaphragm, the liver, and the vertebral line can be seen. On the left, the diaphragm, spleen, and vertebral line should be in view. In a patient without pleural effusion, one should not be able to visualize the lung as it is mostly air and scatters the sound produced by the transducer. However, in the presence of pleural effusion, the area above the diaphragm is filled with fluid and therefore will appear anechoic. In addition, the vertebral line will be present past the diaphragm as the fluid allows the sound waves to propagate and not scatter. This is known as the ‘spine sign’ (also known as the ‘V-line’). Finally, one is often able to see the atelectatic lung float and move with respirations in the fluid, this is known as the ‘sinusoid sign.’ These are the three criteria outlined by consensus statements in the identification of pleural effusions.1 Occasionally, the area above the diaphragm may look like spleen or liver, but this is known as ‘mirror image’ artifact and is normal.2 Figure 2 shows both the right and left views of our patient.

Figure 2: Pleural effusion showing anechoic pleural fluid, atelectatic lung, and ‘spine sign

Accuracy with Ultrasound

Ultrasound is more accurate than either chest x-ray or physical exam in the identification of small pleural effusions.3 For a chest x-ray to identify fluid there usually needs to be more than 200cc present.2 A meta-analysis found that ultrasound had a mean sensitivity of 93% (95%CI: 89-96%) and specificity of 96% (95%CI: 95-98%).4

 

Our patient went on to have a chest x-ray where he was found to have bilateral pleural effusions (see Figure 3).

Figure 3: Bilateral pleural effusions seen on chest radiography in our patient.

In Summary

Three criteria are used to identify pleural effusion on ultrasound; anechoic fluid above the diaphragm, the ability to visualize the spine above the diaphragm (‘spine sign’), and atelectatic lung moving with respirations (‘sinusoid sign’). Lung ultrasound for the detection of pleural effusion is more reliable to identify small effusions in comparison to both radiography and physical exam.


References:

  1. Volpicelli G, Elbarbary M, Blaivas M, et al. International evidence-based recommendations for point-of-care lung ultrasound. Intensive Care Med. 2012;38(4):577-591. doi:10.1007/s00134-012-2513-4.
  2. Liu RB, Donroe JH, McNamara RL, Forman HP, Moore CL. The practice and implications of finding fluid during point-of-care ultrasonography: A review. JAMA Intern Med. 2017;177(12):1818-1825. doi:10.1001/jamainternmed.2017.5048.
  3. Wong CL, Holroyd-leduc J, Straus SE. CLINICIAN ’ S CORNER Does This Patient Have a Pleural Effusion ? PATIENT SCENARIO. Jama. 2010;301(3):309-317. doi:10.1001/jama.2008.937.
  4. Grimberg AI, Carlos Shigueoka DI, Nagib Atallah III Á, et al. Diagnostic accuracy of sonography for pleural effusion: systematic review Acurácia diagnóstica da ultrassonografia nos derrames pleurais: revisão sistemática
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PoCUS – Pneumothorax

Medical Student Clinical Pearl

Vlad Kovalik
MD Candidate, 2019
Dalhousie University Faculty of Medicine

Reviewed and Edited by Dr. David Lewis


A 90-year-old female presented to the emergency department after a fall. Her vitals were stable and a chest x-ray demonstrated three posterior rib fractures. She was keen to be managed at home and had the necessary supports in place. She was discharged with a prescription for analgesics and instructions to return to the ED if her condition changed.

4 days later, the same patient returned to the emergency department with shortness of breath and increased work of breathing. Auscultation revealed decreased air entry on the left. A pneumothorax was at the top of the differential.

PoCUS for Pneumothorax

Lung ultrasound has been found to be more sensitive than chest x-ray for detecting pneumothorax.1 To begin scanning, it is best to have the patient in a supine or semi-recumbent position. The high frequency linear array transducer provides excellent near-field imaging and may be used to better appreciate Lung Sliding, however both the phased array or curvilinear probe may also be used. The probe should be positioned in the longitudinal orientation, with the marker towards the patient’s head, on the anterior chest. Scanning through various rib spaces on both sides completes the exam.

In a normal healthy lung, the visceral and parietal pleura slide against each other creating a distinct shimmering effect known as Lung Sliding. The presence of Lung Sliding rules out pneumothorax with nearly 100% sensitivity in the area directly under the probe.2 *

Lung sliding


Absent lung sliding

Comet-tails are another normal feature of a healthy lung. This is an artifact caused by the reverberation between the parietal and visceral pleura. Comet-tails are seen as bright, vertical lines that fade quickly. The detection of comet tails allows you to rule-out pneumothorax.3

The Seashore Sign is a normal finding in M-mode of a healthy lung. The sliding of the parietal and visceral pleura creates a sand like pattern directly deep to the pleural line. In a pneumothorax, there is air between the parietal and visceral pleura and thus the ultrasound beam is scattered deep to the parietal pleura. In this case, an artifact known as the Barcode Sign may be seen where a reflection of the chest wall is seen below the parietal pleura.5 *

The most specific finding of pneumothorax is the Lung Point Sign. This is the point where the visceral pleura begins to separate from the parietal pleura indicating the boundary of the pneumothorax. Although pathognomonic for pneumothorax it is not always present – the sensitivity is 66%.4

Lung Point

In summary

PoCUS for pneumothorax can be performed quickly at the bedside and is more sensitive than chest x-ray. Look for the absence of Lung Sliding, the absence of Comet-tails and try to locate the Lung Point Sign.

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Decisions: A 20-year-old male with dark stool

Medical Student Clinical Pearl – January 2019

Lucy Eum – Med I Class of 2021, Dalhousie Medicine New Brunswick 

Reviewed and Edited by Dr. David Lewis


Case

A 20-year-old African male presented to the emergency department with black, tarry stool for the past two days. He appeared hemodynamically stable. He was treated for peptic ulcer disease (PUD) due to Helicobacter pylori infection eight months ago after an episode of severe hemorrhage. His medications included ferrous sulfate and Pepto-Bismol. He did not have a primary care provider.

What diagnoses should be considered?

90% of melena is due to upper gastrointestinal (GI) hemorrhage proximal to the ligament of Treitz, but the pharynx and small bowel may sometimes be involved.2 Major causes of upper GI bleeding include PUD, varices, Mallory-Weiss tear, or neoplasms.1 Life-threatening hemorrhage, varices, ulcerations, arteriovenous malformations, and malignancy must also be considered.1

It is important to distinguish between dark stool from blood, known as melena, and dark stool from other causes, such as iron or bismuth. Liquid consistency, shininess, and foul smell are distinct features of melena. 5

What questions should this patient be asked?

Symptoms can help determine the severity and etiology.1 Upper abdominal pain is common with peptic ulcer. Dysphagia combined with weight loss and early satiety is characteristic of malignancy. Significant coughing or retching may lead to Mallory-Weiss tear.2

Comorbidities and prior episodes of upper GI bleeding should be asked. History of liver disease and alcoholism are associated with variceal hemorrhage. Abdominal aortic aneurysm is associated with an aortoenteric fistula. A history of H. pylori infection and NSAID use are risk factors for PUD.2

The use of NSAIDs, antiplatelets, or anticoagulants must be identified. Medications that can induce pill esophagitis (i.e. bisphosphonates) also need to be identified. Bismuth and iron can both lead to harmless darkening of the stool.2

Are any investigations required?

Physical exam begins with an assessment of the patient’s hemodynamic stability.2 Signs of any co-morbidities should be noted. Laboratory tests should include complete blood count, liver function tests, and serum electrolytes. The hemoglobin level may be unchanged from baseline for the first 24 hours.1

Is fecal occult blood test required?

The FOBT has only been validated for use in asymptomatic patients for colorectal cancer (CRC) screening.5 For symptomatic (i.e. melena) patients with high pre-test probability of GI bleeding, the FOBT has a high false positive rate.5

Foods with peroxidase activity (i.e. red meat), vitamin C, antiplatelets and anticoagulants can influence the FOBT results,5 therefore dietary and medication restriction for three days is needed.3 Therefore, the FOBT is unsuitable for emergency rooms despite common use in this setting as a point-of-care (POC) test.3 The newer immunochemical FOBTs do not require dietary restriction and have shown improved accuracy as POC testing for CRC, but its accuracy in evaluating black-coloured stools remains unclear.3, 7

There is speculation that FOBT may be used for patients with dark stools on iron supplementation.3 However, melena is usually well-characterized by its liquid consistency, shininess, and foul smell. Importantly, the FOBT has never been validated for such use to distinguish between melena and other causes of dark stool.3, 5

How should this patient be managed?

A hemodynamically stable patient should be promptly categorized according to rebleeding and mortality risk, using the Glasgow Blatchford Score (GBS) or Rockall Score. They are validated tools based on information such as the patient’s blood pressure, hemoglobin level, and co-morbidities.4, 6

Although pre-endoscopic empiric therapy with PPI is recommended for all patients, this is based on the excellent safety profile of PPIs rather than evidence regarding their efficacy.4 Histamine-2 receptor antagonists are ineffective as preendoscopic therapy.4, 6

Endoscopy within the first 24 hours of presentation is recommended for suspected GI bleeding,1,4 although patients with very low GBS Score (i.e. zero) are unlikely to benefit.5

Generally, all patients with upper GI bleeding require gastroenterology consult. In cases where endoscopy is not suitable, surgical consultation is needed.2

Case revisited

Physical exam and lab results were unremarkable except low hemoglobin, which yielded a total GBS Score of 2 for this patient. Since this is considered high risk1, gastroenterology was consulted. The patient was given an infusion of IV PPI.

Although the patient is on iron and bismuth, he had been on these medications for many months, and, given his history of severe hemorrhage due to PUD without a family physician to provide follow-up care, it was deemed appropriate to investigate further.


References

1. Kim B, Li B, Engel A, Samra J, Clarke S, Norton I et al. Diagnosis of gastrointestinal bleeding: A practical guide for clinicians. World Journal of Gastrointestinal Pathophysiology. 2014;5(4):467.

2. Cappell M, Friedel D. Initial Management of Acute Upper Gastrointestinal Bleeding: From Initial Evaluation up to Gastrointestinal Endoscopy. Medical Clinics of North America. 2008;92(3):491-509.

3. Ip S, Sokoro A, Buchel A, Wirtzfeld D, Konrad G, Fatoye T et al. Use of Fecal Occult Blood Test in Hospitalized Patients: Survey of Physicians Practicing in a Large Central Canadian Health Region and Canadian Gastroenterologists. Canadian Journal of Gastroenterology. 2013;27(12):711-716.

4. Barkun A, Fallone C, Chiba N, Fishman M, Flook N, Martin J et al. A Canadian Clinical Practice Algorithm for the Management of Patients with Non-Variceal Upper Gastrointestinal Bleeding. Canadian Journal of Gastroenterology. 2004;18(10):605-609.

5. Narula N, Ulic D, Al-Dabbagh R, Ibrahim A, Mansour M, Balion C et al. Fecal Occult Blood Testing as a Diagnostic Test in Symptomatic Patients is not Useful: A Retrospective Chart Review. Canadian Journal of Gastroenterology and Hepatology. 2014;28(8):421-426.

6. Barkun A. International Consensus Recommendations on the Management of Patients With Nonvariceal Upper Gastrointestinal Bleeding. Annals of Internal Medicine. 2010;152(2):101.

7. Huddy JR, Ni MZ, Markar SR, Hanna GB. Point-of-care testing in the diagnosis of gastrointestinal cancers: Current technology and future directions. World Journal of Gastroenterology. 2015;21(14):4111.

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Basic ECG Interpretation

Bare Bones Basics of ECG Interpretation from a First Year Medical Student Perspective

Medical Student Clinical Pearl – October 2018

Victoria Kulesza – Med I Class of 2021, Dalhousie Medicine New Brunswick 

Reviewed and Edited by Dr. David Lewis


Physiology

Electrical Events and Corresponding Waves and Lines on a Standard ECG

Basic Interpretation

Common Arrhythmias

Summary

Suggested Resources

References


Physiology

Cardiac cells are electrically polarized in their resting state, with the inside holding a negative charge in comparison to the outside.1,3 Membrane pumps maintain this electrical polarity through the regulation of ions including potassium, sodium, chloride and calcium.1 Depolarization is the key electrical event of the heart that occurs spontaneously in some cells and is initiated by the arrival of an electrical impulse carrying positively charged ions in other cells.1 There are 3 key cells involved in the electrical and mechanical activities that occur within the heart:

 

The sequential depolarization of cells creates a wave of depolarization that transmits across the entire heart, representing a flow of electricity that can be detected by the electrodes placed on the surface of that patient’s body. The waveforms visible on the ECG represent the electrical activity of the myocardial cells, the cells making up the vast majority of the heart.1 At the end of the depolarization process, cardiac cells are repolarized through membrane pumps reversing the flow of ions. Both the depolarization and repolarization are represented as the wave forms on the ECG.1


Electrical Events and Corresponding Waves and Lines on a Standard ECG

P Wave

The heartbeat is initiated in the sinoatrial node located in the posterior wall of the right atrium.4 After the sinus node fires, the atrial myocardium is depolarized in a wave-like fashion causing the atrial contraction. This depolarization and contraction of the atrial myocardial cells results in the first P wave.1 The wave of depolarization does not immediately pass through to the ventricles, the atrioventricular node located at the floor of the right atrium, slows the conduction of the electrical impulse to allow the atria to fully complete their contraction. 1,4 The contraction of the atria forces blood from the atria through the atrio-ventricular valves, known as the tricuspid and mitral valves, into the ventricles.3

PR Interval

This interval is the time that is required for the electrical impulse to travel from the atria, through the AV node, bundle of His, bundle branches and Purkinje fibers to the point where the ventricular myocardium begins its depolarization.5 As blood flows through the AV valves the physiologic pause in electrical conduction is represented on the EKG as the flat line following the initial P wave. The ventricular conduction system is composed of 3 parts including the Bundle of His, Bundle Branches and the Terminal Purkinje Fibers.1 The ventricular depolarization is rapidly transmitted through the Bundle of His which emerges from the AV node and subsequently bifurcates into the left and right bundle branches which carry the impulse down the interventricular septum to their terminating fascicles in multiple Purkinje fibers.1,3 Once this current is delivered to the ventricular myocardium the depolarization causes ventricular contraction visible on the ECG as the QRS complex.1

PR Segment

A straight line between the end of the P wave and the start of the QRS complex reflects the time between the end of atrial depolarization and the start of ventricular depolarization.1

QRS Complex

The QRS complex consists of 3 individual waves in a normal conduction1,3:

  • Q Wave: first deflection downward
  • R Wave: first upward deflection
  • S Wave: first downward deflection subsequent to an upward deflection

A complete QRS complex represents ventricular depolarization as well as the initiation of ventricular contraction.1,3 The use of the term QRS Interval describes the duration of the QRS complex alone indicating the duration of ventricular depolarization specifically.1

ST Segment

A straight line between the end of the QRS complex and the beginning of the T wave known as the ST segment measures the time from the end of ventricular depolarization to the beginning of repolarization.1

T Wave

Following the depolarization of the myocardial cells, there is a short refractory period and subsequent recovery phase identified as the T wave on the ECG.1,3,5 This is phase of ventricular repolarization that begins after the QRS and is completed at the end of the T wave.3,5 Repolarization is a slower process than the depolarization which is illustrated by the broader nature of the T wave in comparison to the QRS.1,5

QT Interval

This interval includes the QRS complex, ST segment as well as the T wave which allows for the measurement of time between the beginning of ventricular depolarization to the end of ventricular repolarization.


 

Basic Interpretation

The most effective way to ensure clinically significant abnormalities are not missed on ECG is to develop a consistent order of analysis. One suggested order is as follows:

 

A. Determine Rate:

  1. Sinus Tachycardia = >100 BPM
  2. Sinus Bradycardia = <60 BPM
  3. Three Ways to Determine Rate:
    • Identify an R wave that falls on or near one of the heavy lines of the ECG strip, count the number of large squares between this first R wave and the beginning of the subsequent wave. Divide 300 by the number of large squares between the R waves to determine the number of cardiac cycles per minute. Counting the number of small squares between R waves and dividing 1500 by this number would identify with greater accuracy the heart rate.1
    • Identify the series of small pink indicators above the rhythm strip that identify 3 second intervals and count the number of cycles between two 3 second intervals – multiply this number by 10 to identify the number of beats per minute.1
    • In the event of an irregular heartbeat identify the number of QRS complexes and multiply this number by 6. Each started ECG paper reads at 25mm/s therefore 1 ECG represents 10 seconds of activity.2

Thaler 2015

 

B. Intervals:

Identify the length of the PR and QT Intervals as well as the width of the QRS complexes

Normal Interval Lengths5:

  1. PR = 0.12 – 0.20 sec
  2. QT = varies with overall heart rate
  3. QRS = 0.05 – 0.10 sec

 

 

 

 

 

 

 

C. Rhythm5:

  1. P waves present and normal?
  2. QRS complexes wide or narrow? General pattern – regular, regularly irregular or irregularly irregular?
    1. Wide = >0.12 sec
    2. Narrow = <0.12 sec
  3. Relationship between P waves and QRS complexes
  4. Overall rhythm regular or irregular?

 

D. Axis

  1. The ECG electrodes record the average direction of flow of electrical current within the heart.
  2. Lead I is the zero reference point, any axis lying below is deemed positive while those lying above are deemed negative.
  3. When the wave of depolarization begins, any lead that views this wave as moving towards it will record this as a positive deflection on the ECG paper.
  4. Assessment of P Wave Axis:
    • Atrial depolarization begins at the sinus node in the right atrium and follows a right to left and inferior direction. This depolarization of the right to left atria should demonstrate a positive deflection in leads aVL, I, II and aVF.
  5. Assessment of QRS Complex Axis:
    • As the wave of depolarization moves through the interventricular septum the current moves in a left to right direction. This wave may not be visible on the ECG but when apparent appears as a negative deflection in leads I, aVL (V5 and V6). As a result of the increased size of the left ventricle in comparison to the right, the remainder of the QRS complex vector of flow is directed leftward and is demonstrated as the positively deflected R wave in most left lateral and inferior leads. The aVR lead will record a deep negative deflection based on the direction of flow being away from this lead.

 


 

Common Arrhythmias1

1. Sinus Tachycardia

  • HR >100 bpm
  • Can be normal or pathologic, strenuous exercise can cause HR above 100.

 

2. Sinus Bradycardia

  • HR <60 bpm
  • Can be normal or pathologic, many well-conditioned athletes maintain a resting HR below 60.

 

3. Paroxysmal Supraventricular Tachycardia

  • HR 150-250 bpm
  • Narrow complex QRS
  • Very common, sudden onset, sudden termination.
  • Clinical Symptoms: palpitations, shortness of breath, dizziness. Possibly induced by alcohol, caffeine or extreme excitement.

 

4. Atrial Flutter

  • P waves 250-350 bpm
  • Atrial depolarization occurs so rapidly that discrete P waves are indiscernible.
  • Leads II and III demonstrate a prominent saw-tooth
  • AV node cannot handle the number of atrial impulses therefore there is an unequal number of P waves to QRS complexes – some electrical impulses from the sinus node bump into a refractory node and go no further, this is called AV Block. 2:1 block is most common while 3:1 and 4:1 are also frequently observed.
  • Clinical Symptoms: shortness of breath, angina type discomfort.

 

 

5. Atrial Fibrillation

  • AV Node may receive >500 impulses per minute
  • More common than atrial flutter, most commonly sustained arrhythmia.
  • No true P waves are discernible, AV node allows occasional impulses to pass through to the ventricles, creating an irregularly irregular ventricular rate often in the range of 120-180 bpm.
  • Clinical Symptoms: some patients experience no symptoms, others experience shortness of breath, chest pain, palpitations and dizziness.

 

6. Premature Ventricular Contractions

  • Most common ventricular arrhythmia.
  • Retrograde P wave or no P wave prior to the QRS.
  • Wide QRS of at least 0.12 seconds in majority of the leads often followed by a compensatory pause before the subsequent beat.
  • Often occur randomly and rarely require treatment unless an isolated PVC is noted in the setting of acute MI as it may trigger ventricular tachycardia or ventricular fibrillation.
  • When to worry:
    • Frequent PVCs
    • Consecutive runs, 3+ in a row
    • Multiform – demonstrating variation in the site of origin
    • Occurring on the T wave – “R-on-T” phenomenon
    • PVC in the setting of an acute MI

 

 

7. Ventricular Tachycardia

  • Rate 120-200 bpm
  • Wide complex QRS
  • A run of 3+ consecutive PVCs.
  • Prolonged ventricular tachycardia is an emergency requiring immediate treatment to prevent cardiac arrest.
  • May be uniform or polymorphic, uniform being more closely associated with healed infarctions and polymorphic waveforms more commonly associated with acute coronary events.

 

8. Ventricular Fibrillation

  • Spasmodic tracings or coarse ventricular fibrillation or fine ventricular fibrillation without any true QRS complexes.
  • Heart generates no cardiac output, CPR and defibrillation are required immediately.
  • Most common arrhythmia in adults who experience sudden death.
  • Common predisposing factors:
    • Myocardial ischemia/infarction
    • Heart failure
    • Electrolyte disturbances
    • Hypoxemia or hypercapnia
    • Hypotension or shock
    • Overdoses of stimulants especially when used in combination with others

 


 

Summary

 


 

 


 

Suggested Resources

Teaching Medicine – Rhythm Strip Interpretation Practice

ECG Guide Mobile Smartphone App

  • Available through itunes app store

The Only EKG Book You’ll Ever Need

  • PDF available online through Dalhousie Library

 

References

  1. Thaler, M. S. (2015). The Only EKG Book You’ll Ever Need (9th ed.). Lippincott, Williams & Wilkins.
  2. Andrade, J. (2013). ECG Guide [Mobile application software]. Retrieved from http://itunes.apple.com
  3. Dubin, D. (2000). Rapid interpretation of EKG’s: An interactive course (6th ed.). Tampa, Fla.: Cover Pub.
  4. McKinley, M. P., OLoughlin, V. D., Harris, R. T., & Pennefather-O’Brien, E. E. (2015). Human anatomy (4th ed.). New York, NY: McGraw-Hill Education.
  5. Khan, M. (2008). Rapid ECG interpretation (3rd ed., Contemporary cardiology (Totowa, N.J). Totowa, N.J.: Human Press.
  6. Thomas, V. (n.d.). Premature Ventricular Contractions Treatment Cape Town. Retrieved from https://cardiorhythm.co.za/premature-ventricular-contractions/
  7. https://inside.fammed.wisc.edu/medstudent/pcc/ecg/axis.html
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PoCUS and Clavicle Fractures

Using PoCUS to diagnose clavicular fractures

Medical Student Clinical Pearl – May 2018

Danielle Rioux – Med III Class of 2019, Dalhousie Medicine New Brunswick 

Reviewed by Dr. Mandy Peach and Dr. David Lewis

Case: A 70 year-old man presented to the emergency department with pain in his left shoulder and clavicular region following a skiing accident. He slipped and fell on his left lateral shoulder while he was on skis at the ski hill. He has visible swelling in his left shoulder and clavicular region, and was not able to move his left arm.

On exam: The patient was in no sign of distress. He was standing and holding his left arm adducted close to his body, supporting his left arm with his right hand. There was swelling and ecchymosis in the left clavicle, mid-shaft region, with focal tenderness. On palpation, there was crepitation, tenderness, swelling, and warmth in this region. He was unable to move his left shoulder due to pain. His neurovascular exam on his left arm was normal. Auscultation of his lungs revealed normal air-entry, bilaterally and no adventitious sounds.

Point of Care Ultrasound (PoCUS): We used a linear, high-frequency transducer and placed it in the longitudinal plane on the normal right clavicle (see Image 1.), and the fractured left clavicle (see Image 2.). Image 3 shows the fractured clavicle in the transverse plane.

Image 1. PoCUS of normal right clavicle along the long axis of the clavicle (arrows depict the hyperechoic superficial cortex with deep acoustic shadowing).

Clip 1. PoCUS of normal right clavicle along the short axis of the clavicle. The transducer is moving from the lateral to medial, note the visible hyperechoic curved superficial cortex and the subclavian vessels at the end of the clip. 

Image 2. PoCUS of normal right clavicle along the short axis of the clavicle (arrows depict the hyperechoic superficial cortex with deep acoustic shadowing).

Image 3. PoCUS of a fracture in the left clavicle along the long axis of the clavicle

Clip 2. PoCUS of a fracture of the left clavicle, viewed in the long axis of the clavicle. Compare this view with image 1.

Clip 3. PoCUS of a fracture in the left clavicle viewed in the short axis of the clavicle. Compare this view with Clip 1. Note the fracture through the visible cortex and the displacement that becomes apparent halfway through the clip.

Radiographic findings: Radiographic findings of the left clavicle reveal a mid-shaft spiral clavicular fracture.  (Image 4).

Image 4. Radiographic image of fractured left clavicle.

 

Take home point: Research has shown that Ultrasonography is a sensitive diagnostic tool in the evaluation of fractures (Chapman & Black, 2003; Eckert et al., 2014; Chen et al., 2016).

This case provides an example of how PoCUS can be used to diagnose clavicle fractures in the emergency department. In a rural or office setting where radiography is not always available, PoCUS can be used to triage patients efficiently into groups of those with a fracture and those with a low likelihood of a fracture. This would enable more efficient medical referrals while improving cost-effectiveness and patient care.

References:

Chapman, D. & Black, K. 2003. Diagnostic musculoskeletal ultrasound for emergency physicians. Ultrasound, 25(10):60

Eckert, K., Janssen, N., Ackermann, O., Schweiger, B., Radeloff, E. & Liedgens, P. 2014 Ultrasound diagnosis of supracondylar fractures in children. Eur J Trauma Emerg Surg., 40:159–168

Chen, K.C., Chor-Ming, A., Chong, C.F. & Wang, T.L. 2016. An overview of point-of-care ultrasound for soft tissue and musculoskeletal applications in the emergency department, Journal of Intensive Care, 4:55

This post was copyedited by Dr. Mandy Peach

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