Friday Board Review

Board Review with Dr. Edward Guo

A 30 year old male with a history of active IVDU and previous MRSA endocarditis is presenting with tooth pain that has been worsening over several days. He denies fever, chest pain, or shortness of breath. Vital signs are: Temp 99.0F, HR 86, BP 148/76, RR 16, SpO2 98% RA. Exam shows track marks in the antecubital fossas bilaterally and no appreciable cardiac murmur. He has poor dentition overall with an appreciable area of fluctuance above the gums of tooth #4. Which of the following is appropriate management for this patient?

A: administer IV vancomycin followed by ED incision and drainage then discharge

B: consult oral maxillofacial surgery for drainage

C: draw blood cultures and admit for IV antibiotics

D: perform ED incision and drainage and discharge with clindamycin

Answer: administer IV vancomycin followed by ED incision and drainage then discharge

Patients with a history of prosthetic heart valves or infective endocarditis among other cardiac conditions are considered high-risk for developing endocarditis with dental procedures and surgical procedures on infected skin. In this patient, incision and drainage of the periapical abscess should be performed 30 to 60 minutes after receiving a dose of antibiotics with coverage against MRSA. OMFS does not need to be consulted for abscess drainage. There are no systemic symptoms such as fever at this time to suggest bacteremia for admission. 

Table copied from Tintinalli’s

References:

Brenner D, & Marco C.A., & Rothman R.E. (2020). Endocarditis. Tintinalli J.E., & Ma O, & Yealy D.M., & Meckler G.D., & Stapczynski J, & Cline D.M., & Thomas S.H.(Eds.), Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw Hill.

Wednesday Image Review

What’s the Diagnosis? By Dr. Ravi Tata

A 65 year old female with past medical history significant for recently diagnosed COPD presenting with shortness of breath. She has been symptomatic for the past month but has been getting progressively worse over the past couple weeks. She is medically compliant with her prescribed inhalers and is not on supplemental oxygen at home. She also reports worsening bilateral lower extremity edema and fatigue over the past two days.

Patient has an initial pulse oximetry of 65% in triage on room air, placed on non-rebreather and improved to 85%. Other vitals are as follows: BP 122/87, HR 101, Temp 97.4, RR 18. Physical exam significant for tachycardia, respiratory distress with poor air movement bilaterally, and bilateral lower extremity pitting edema from the knees down. A focused cardiopulmonary point-of-care ultrasound is shown below. What’s the likely diagnosis and abnormal ultrasound finding?

Answer: COPD with pulmonary hypertension and right heart strain

  • Shown by dilated right ventricular outflow tract (RVOT) on PSLA and D-sign on PSSA.
  • Normally in PSLA, the RV outflow tract, aortic outflow tract, and L-atrium should be roughly the same size. Additionally, in PSSA the LV is normally bowing into the RV due to the increased pressures comparatively. When there is right heart strain, the RV dilates from the increased pressure and pushes the interventricular septum back to the midline, creating the “D-sign”.
    • This is most concerning for pulmonary embolism in the acute setting. This patient had a CTA chest performed which was negative for pulmonary embolism.
  • Right heart strain is also congruent in the setting of long-standing, untreated COPD leading to pulmonary hypertension causing her shortness of breath and bilateral lower extremity edema without pulmonary edema.
  • When seeing an acutely ill patient like this at bedside, it is important to rule out the most life-threatening pathology with the information you have readily available. While the acute-on-chronic nature of her story may support a diagnosis of COPD causing chronic pulmonary hypertension and right heart strain, a pulmonary embolism must be ruled out in the setting of hypoxia and right heart strain on POCUS as it would require more emergent intervention and can also be concurrently present.

References:

https://www.pocus101.com/the-d-sign-right-heart-strain-from-pressure-vs-volume-overload/

Falster C, Egholm G, Wiig R, Poulsen MK, Møller JE, Posth S, Brabrand M, Laursen CB. Diagnostic Accuracy of a Bespoke Multiorgan Ultrasound Approach in Suspected Pulmonary Embolism. Ultrasound Int Open. 2023 Jan 16;8(2):E59-E67. doi: 10.1055/a-1971-7454. PMID: 36726389; PMCID: PMC9886498.

Tuesday Advanced Cases & Procedure Pearls

Pediatric Chest Pain by Dr. Edward Guo

Case: An 18 year old female with a past medical history of anxiety, 2 weeks post-op from tonsillectomy presents for chest pain. She woke up today with severe, non-radiating central chest pain. Her daily medications include sertraline and oral contraceptives. Vitals are BP 118/86, HR 119, Temp 97.7F, RR 24, SpO2 96% on room air. On exam, she is uncomfortable appearing and tearful. Her oropharynx is clear without signs of erythema or drainage. She is tachycardic without murmurs and has clear lung sounds bilaterally. There are no signs of lower extremity swelling. EKG and point-of-care cardiac ultrasound are shown below:

EKG interpretation: Sinus tachycardia with rightward axis and T wave inversions in anterior leads

POCUS interpretation: Normal LV ejection fraction. No pericardial effusion. Elevated RV to LV ratio. Dilated IVC with < 50% collapse with inspiration. RV free wall hypokinesis with apical hyperkinesis. Tricuspid annular plane systolic excursion 1.0 cm.

Case continued:  Due to high concern for pulmonary embolism, the patient is empirically started on heparin. CTA chest results with acute pulmonary embolism with right heart strain. High sensitivity troponin results markedly elevated at 306 mg/dL. Patient is admitted to the ICU with interventional cardiology consultation. Patient underwent pulmonary arteriogram which demonstrated elevated PA pressures without need for thrombectomy and was discharged in good condition on hospital day #4.

Pearls:

  • Infants and toddlers can have normal T wave inversions in the anterior leads known as “juvenile T waves” which should turn upright by age 7.
    • Any T wave inversion in these leads after they have flipped upright is abnormal.
  • While the S1Q3T3 EKG finding is classically associated with pulmonary embolism, more common EKG findings suggestive of PE include sinus tachycardia, rightward axis, incomplete right bundle branch block, and T wave inversions in the anterior leads.
  • Empirically start anticoagulation in patients with high concern for pulmonary embolism prior to definitive imaging.
  • Right ventricular free wall hypokinesis with apical hyperkinesis is known as McConnell’s sign and is pathognomonic for acute pulmonary embolism.
    • Other POCUS findings include an RV:LV ratio > 1 which is sensitive but not specific. A tricuspid annular plane systolic excursion (TAPSE) < 17 mm is a quantitative measure to diagnose right heart dysfunction on echocardiogram.

References:

Kline JA. Venous Thromboembolism Including Pulmonary Embolism. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw Hill; 2020.

Goodacre, S., & McLeod, K. (2002). ABC of clinical electrocardiography: Paediatric electrocardiography. BMJ (Clinical research ed.)324(7350), 1382–1385. https://doi.org/10.1136/bmj.324.7350.1382

Alerhand S, Hickey SM. Tricuspid Annular Plane Systolic Excursion (TAPSE) for Risk Stratification and Prognostication of Patients with Pulmonary Embolism. J Emerg Med. 2020;58(3):449-456. doi:10.1016/j.jemermed.2019.09.017

Friday Board Review

From the EMDaily Archives: Board Review by Dr. Courtney Martin

A 50 year old male with past medical history of hypertension, type 2 diabetes, and coronary artery disease with multiple prior stents presenting with shortness of breath and fatigue. Vitals demonstrate BP 70/50, HR 79 bpm, RR 26, O2 sat 88% on room air, Temp 36C. On exam, the patient has bilateral rales and 2+ pitting edema. Heart sounds are muffled. Distal pulses are weak, and extremities are cool to the touch. Bedside echocardiogram demonstrates significantly decreased cardiac output with minimal ventricular wall motion. EKG demonstrates ST elevations in anterior leads. What is the most appropriate vasopressor to initiate at this time?

A: dobutamine

B: dopamine

C: epinephrine

D: norepinephrine

E: phenylephrine

Answer: norepinephrine

This patient is demonstrating signs of cardiogenic shock in the setting of acute myocardial infarction. The most common cause of cardiogenic shock is acute ischemia. Other causes include valvular malfunctions, ventricular septal defect, ventricular free-wall rupture, right ventricular infarction, myocarditis, septic shock, arrhythmia, toxicity. The initial step in this case is correction of acute ischemia by activating the cath lab or thrombolytics depending on your facility. In regards to vasopressors, studies have demonstrated norepinephrine is most beneficial in patients with profound hypotension. Dopamine was traditionally used, however, it may increase heart rate and worsen cardiac demand. Epinephrine should be avoided if possible due to increased vasoconstriction with ischemia and arrhythmias. Dobutamine has inotropic effects that are beneficial for cardiac output but does not improve systemic vascular resistance. The combination of norepinephrine and dobutamine may be considered as well. 

References:

Hochman JS, Buller CE, Sleeper LA, et al. Cardiogenic shock complicating acute myocardial infarction–etiologies, management and outcome: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK?. J Am Coll Cardiol. 2000;36(3 Suppl A):1063-1070. doi:10.1016/s0735-1097(00)00879-2

Thursday Conference Content & EKG Review

From the EMDaily Archives: Thrombolytics in STEMI by Dr. Katie Nowlan

Fibrinolysis:

  • In the absence of contraindications, should be given to STEMI patients with symptoms <12 hours when it is anticipated that primary PCI cannot be performed within 120 minutes of first medical contact (class I recommendation) 
  • Up to 12-24 hours of symptoms with STEMI when PCI unavailable (class IIa recommendation)

When to choose thrombolytics? 

  • Non-PCI capable hospital and the total time it would take to transfer to a PCI-capable hospital and first medical contact–device time is > 120 min away
  • Ideally administered within the first 30 minutes of presentation

Thrombolytic agents:

  • tPA: 15 mg IV over 1-2 min, followed by 50 mg IV over 30 min, followed by 35 mg IV over 60 min (total 100 mg over 1.5 hours)
  • TNKase: 30-50 mg IV over 5 sec (dosing is weight based) 
  • rPA: 10 Units x 2 given 30 min apart 

Absolute contraindications:

  • Any prior intracranial hemorrhage
  • Ischemic stroke within 3 months (except acute ischemic stroke within 4.5 hrs) 
  • Known structural cerebral vascular lesion (e.g. AVM) or intracranial neoplasm (primary or metastatic) 
  • Active bleeding or bleeding diatheses (excluding menses)
  • Intracranial or intraspinal surgery within 2 months
  • For streptokinase, prior treatment within the previous 6 months
  • Significant closed-head or facial trauma within 3 months
  • Suspected aortic dissection
  • Severe uncontrolled hypertension unresponsive to emergency therapy

Adjunctive Therapies to thrombolytics:

  • Aspirin: 162 to 325 mg loading dose 
  • Clopidogrel: 300 mg for ≤75 years old; 75 mg for >75 years old 
  • Unfractionated heparin bolus or enoxaparin or fondaparinux

Final points:

  • Transfer! Regardless of hemodynamics or reperfusion success, it is reasonable to still get patients to a PCI-capable center.
  • Angiography recommended within the first 24 hours but AVOIDED for the first 2-3 hours after fibrinolytic therapy.
Wednesday Image Review

What’s the Diagnosis? By Dr. Shivani Talwar

A 34 year old male presenting to the emergency department for left shoulder pain. The pain is constant and worse with movement. He frequently has been feeling similar pain but was in a motor vehicle accident yesterday that exacerbated the pain. He was noted to have a left shoulder deformity with intact range of motion at the shoulder. What’s the diagnosis and treatment?

Answer: Grade III acromioclavicular joint separation; immobilize with a sling for 6-12 weeks and follow up with orthopedic surgery.

Grade Ligament involvementX-ray Findings and ExamTreatment
I– AC ligament sprain
– No instability of clavicle
Exam: Tenderness over AC joint    

X-ray: Normal imaging
Ice, rest, analgesics, immobilization

Early range of motion 1-2 weeks
II– AC ligament rupture
– Sprain of coracoclavicular ligament
Exam: Tenderness and mild step off of AC joint

X-ray: Clavicle elevated 25-50% above acromion, widening of the AC joint
Ice, rest, analgesics, immobilization

Early range of motion 1-2 weeks
III– AC ligament rupture
– Coracoclavicular ligaments partially ruptured
– Deltoid and trapezius muscles detached
Exam: Shoulder droops, prominent distal clavicle

X-ray: Clavicle elevated 100% above acromion, widening of coracoclavicular space
Conservative with sling immobilization

Some cases may be operative
IV– AC joint dislocation with AC ligament rupture
– Complete or partial rupture of coracoclavicular ligament
– Clavicle displaced posteriorly
Exam: Posterior displacement of clavicle

X-ray: Axillary radiograph required to see posterior dislocation
Surgical repair
V– AC joint dislocation with AC ligament rupture
– Complete rupture of coracoclavicular ligament
Exam: Gross clavicular deformity

X-ray: AC joint dislocated, coracoclavicular interspace with 200-300% disparity
Surgical repair
VI– AC joint dislocation with AC ligament rupture
– Intact coracoclavicular ligament
– Clavicle displaced inferiorly
– Intact, partial or complete deltoid and trapezius detachment
Exam: Severe swelling  

X-ray: AC joint dislocated, clavicle displaced inferiorly
Surgical repair
Rockwood Classification of AC Joint Separation

References:

Gorbaty JD, Hsu JE, Gee AO. Classifications in Brief: Rockwood Classification of Acromioclavicular Joint Separations. Clin Orthop Relat Res. 2017 Jan;475(1):283-287. doi: 10.1007/s11999-016-5079-6. Epub 2016 Sep 16. PMID: 27637619; PMCID: PMC5174051.

Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9th Edition. Bjoerson, L. Ebinger, A. Chapter 271. Page 1824-1826. McGraw Hill Professional, 22 Oct. 2019.

Tuesday Advanced Cases & Procedure Pearls

From the EMDaily Archives: BRASH Syndrome by Dr. Richard Byrne

Case: A 69 year old male with a past medical history of hypertension and type 2 diabetes arrives via EMS for chest pain and weakness. EMS found patient with a heart rate of 30, systolic BP 100, awake and and alert. Vitals upon arrival to the ED are BP 92/41, HR 42, Temp 97.7F, RR 20, SpO2 98% on room air. On exam, he is conversant with bradycardia and clear lung sounds. EKG is shown below:

EKG interpretation: sinus bradycardia with left bundle branch block pattern, Sgarbossa criteria negative

Differential diagnosis: acute cardiac ischemia, hyperkalemia, medication overdose (beta blockers, calcium channel blockers, digoxin, clonidine)

Management:

  • Transcutaneous pacer pads
  • 1 mg atropine given with no response
  • 500 mL IV fluid bolus improved SBP to 100
  • Cardiology consult with concerns for acute ischemia given chest pain and new left bundle branch block with bradycardia

Case continued: 40 minutes after arrival, patient suffered a brady-asystolic cardiac arrest. ACLS was started immediately and 1 mg epinephrine and 1 g calcium gluconate were administered. ROSC was achieved with 3 minutes, and patient became awake and alert. Critical lab values resulted with a potassium of 7.7 and creatinine of 3.7 (unknown baseline). The patient was admitted to the ICU on vasopressors, maintained adequate urine output, and did not require emergent hemodialysis. He was discharged in good condition two days later.

Diagnosis: BRASH Syndrome – Bradycardia, Renal failure, AV nodal blocking agents (beta blockers in this case), Shock, and Hyperkalemia

  • Check out this excellent summary of BRASH syndrome from the Journal of Emergency Medicine here.

Pearls:

  • Hyperkalemia is a common cause of bradycardia.
  • Unstable patients should be treated empirically with IV calcium while waiting for lab confirmation.
  • A VBG with lytes may provide a faster laboratory confirmation, though the specimen may have unrecognized hemolysis.
  • The combination of acute renal failure (sometimes from vomiting/diarrhea) in conjunction with AV nodal blocking agents may result in BRASH syndrome.
  • Acute treatment is aimed as for management of hyperkalemia and emergency hemodialysis may be required if patient is anuric or unresponsive to treatment.

References:

Farkas, Joshua et al. BRASH Syndrome: Bradycardia, Renal Failure, AV Blockade, Shock, and Hyperkalemia. Journal of Emergency Medicine 59 (2); 216-223.

Monday Back to Basics & Pharmacology

From the EMDaily Archives: Informed Consent by Dr. Kat Kaminski

Emergency Medicine physicians are expert diagnosticians, resuscitationists, and proceduralists. The process of obtaining informed consent from patients in our care is also an important part of our practice. The exception is acutely life-threatening situations when timely action is required to prevent death or serious harm, whereby consent is implied.

There are 3 components of informed consent in medicine:

  1. Patient capacity to make a treatment decision
  2. Information regarding the patient’s current condition, treatment options, and associated risks and benefits
  3. Voluntary consent to treatment without coercion

Some pearls regarding informed consent:

  • A signed informed consent form provides evidence that the discussion occurred but does not necessarily prove what was discussed.
  • Consent can be revoked by the patient at any time for any reason, and past consent does not imply future consent for a similar procedure.
  • Be honest with the patient about your level of expertise.
  • If appropriate and desired by the patient, involve the patient’s family in the discussion.
  • Unsure if the patient is on the same page? Use teach-back methodology, i.e. “Tell me what you know about this procedure after what we’ve discussed.”

These conversations are not easy in the chaotic ED, where time is extremely limited, and our patients are usually meeting us for the first time. This underscores the importance of gaining trust early in the physician-patient relationship – a skill cultivated by communicative and compassionate Emergency Medicine physicians.

References:

1. Magauran, B. (2009). Risk management for the emergency physician: competency and decision-making capacity, informed consent, and refusal of care against medical advice. Emergency Medicine Clinics of North America., 27(4), 605–14, viii. https://doi.org/10.1016/j.emc.2009.08.001

2. Moore, G. P., Moffett, P. M., Fider, C., & Moore, M. J. (2014). What emergency physicians should know about informed consent: legal scenarios, cases, and caveats. Academic emergency medicine: official journal of the Society for Academic Emergency Medicine21(8), 922–927.