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. 

Friday Board Review

Board Review with Dr. Edward Guo

A 70 year old male with a past medical history coronary artery disease, heart failure with reduced ejection fraction, and severe aortic stenosis presents via EMS for shortness of breath. History is limited due to acute respiratory distress while patient is on CPAP. Vital signs are: BP 88/60, HR 120, T 36.7, RR 30, SpO2 90% on PEEP 8 and FiO2 100%. On exam, he is in severe respiratory distress with accessory muscle usage and speaks in 2 word phrases. There is a prominent systolic ejection murmur over the right second intercostal space. Rales are heard at the lung bases bilaterally, and there is 4+ pitting edema of the lower extremities. EKG shows sinus tachycardia. Which of the following is the preferred resuscitation strategy to optimize hemodynamics prior to intubation? 

A: bolus 1 liter isotonic fluids

B: epinephrine infusion 

C: norepinephrine infusion

D: phenylephrine infusion

E: push dose epinephrine prior to induction

Answer: phenylephrine infusion

This patient is presenting in acute hypoxic respiratory failure likely secondary to pulmonary edema related to acute on chronic heart failure. Patients with severe aortic stenosis are preload dependent to maintain coronary and systemic perfusion. Thus, typical management with positive airway pressure and nitrates should be used cautiously. In hypotensive patients with aortic stenosis, phenylephrine is the vasopressor of choice due to its pure alpha-1 agonist effects to increase diastolic blood pressure and coronary perfusion. Reflex bradycardia is also beneficial to allow for more diastolic filling time. Inotropes such as epinephrine are not recommended due to tachycardia and increased myocardial oxygen demand. Norepinephrine is a reasonable alternative but not the preferred agent. Fluid administration is likely to worsen this patient’s hemodynamics and respiratory status by volume overload.

References:

Goertz AW, Lindner KH, Schutz W, Schirmer U, Beyer M, Georgieff M. Influence of phenylephrine bolus administration on left ventricular filling dynamics in patients with coronary artery disease and patients with valvular aortic stenosis. Anesthesiology. 1994;81(1):49-58.

Wednesday Image Review

From the EMDaily Archives: What’s the Diagnosis? By Dr. Eric Chavis

A 27 year old male with a history of osteosarcoma with numerous lung metastases s/p left upper lobe wedge resection 1 year ago presents with dyspnea on exertion and “abnormal findings on outpatient CT scan”. Vitals include HR 135, RR 18, SpO2 93% on room air. On exam, he has diminished but present breath sounds bilaterally. A chest x-ray is obtained and shown below. What’s the diagnosis?

Answer: Hydropneumothorax (see pleural line in periphery of left lung and pleural effusion)

  • Defined as the presence of both air and fluid in the pleural space
  • Can be either atraumatic or traumatic (hemopneumothorax)
  • Underlying etiologies can include: COPD (due to presence of blebs), pneumonia, TB, malignancy, prior lung instrumentation
  • Most common presenting symptoms are SOB and cough
  • Diagnosis can be made on CXR, US, or CT
  • In the event of tension physiology, treat as tension PTX with needle decompression, tube thoracostomy
  • For more stable cases, treatment is supplemental O2 to help with lung re-expansion, tube thoracostomy, and pulmonology consultation
  • Ultimately, requires admission for further workup, treatment of underlying condition
  • The etiology of this patient’s hydropneumothorax was unknown, but possibly related to underlying malignancy


References:

Kasargod V, Awad NT. Clinical profile, etiology, and management of hydropneumothorax: An Indian experience. Lung India. 2016;33(3):278-280. 

Friday Board Review

Board Review with Dr. Edward Guo

A 64 year old male with a past medical history of diabetes mellitus, coronary artery disease, and congestive heart failure is being evaluated for chest pain. His initial vital signs are within normal limits. His EKG is unchanged from previous showing a narrow-complex sinus rhythm. While he is in the emergency department, he reports feeling palpitations. The cardiac monitor records a monomorphic, wide-complex tachycardia at a rate of 140 beats/minute while his blood pressure is 132/80. What is the first-line medication for treatment of this patient’s condition?

A: adenosine

B: amiodarone

C: epinephrine

D: magnesium sulfate

E: procainamide

Answer: procainamide

This patient with a history of extensive cardiac disease is likely experiencing stable ventricular tachycardia (VT). The PROCAMIO study in 2017 demonstrated that procainamide is likely superior to amiodarone for termination of wide-complex tachycardia and associated with fewer major adverse cardiac events. Adenosine is commonly used in the management of supraventricular tachycardias but is unlikely to terminate a tachycardia of ventricular origin. Epinephrine is used for pulseless VT as part of the ACLS algorithm. Magnesium sulfate is used for polymorphic VT also known as Torsades De Pointes but is not first-line for monomorphic VT.

References:

Ortiz, M., Martín, A., Arribas, F., Coll-Vinent, B., Del Arco, C., Peinado, R., Almendral, J., & PROCAMIO Study Investigators (2017). Randomized comparison of intravenous procainamide vs. intravenous amiodarone for the acute treatment of tolerated wide QRS tachycardia: the PROCAMIO study. European heart journal38(17), 1329–1335. https://doi.org/10.1093/eurheartj/ehw230

Wednesday Image Review

What’s the Diagnosis? By Dr. Dan Harwood

A 52 year old female presents via EMS after being found down outside. Medical history is notable for reported insulin-dependent diabetes. The patient is found to have altered mental status on presentation, and is unable to provide further history. Vitals are notable for heart rate of 138, blood pressure 92/50, and temperature of 102.1F; POC blood glucose shows blood sugar over 600. On physical exam, patient is found to have hemorrhagic bullae of her left lower extremity with palpable crepitus. Labs in the emergency department are notable for WBC of 36k, anion gap of 30, and lactate of 2.5.

Point-of-care ultrasound of the left lower extremity is shown below. What is the most likely diagnosis, and what findings on the ultrasound imaging support this?

Answer: Necrotizing Fasciitis; “dirty shadowing”

  • Subcutaneous air results will appear as hyperechoic lines on soft tissue ultrasound, with “dirty shadowing” of tissue/structures deep to the air.
  • These hyperechoic lines are seen at the borders between air and soft-tissue, due to a scattering of ultrasound waves that occurs at these boundaries.
  • Additional findings of necrotizing fasciitis on ultrasound include a “cobblestone” appearance of the subcutaneous tissue with abnormal fluid collections. These findings are not specific to necrotizing fasciitis, however.

References:

Tso DK, Singh AK. Necrotizing fasciitis of the lower extremity: imaging pearls and pitfalls. Br J Radiol. 2018 Jul;91(1088):20180093. doi: 10.1259/bjr.20180093. Epub 2018 Mar 28. PMID: 29537292; PMCID: PMC6209465.

Buttar S, Cooper D Jr, Olivieri P, Barca M, Drake AB, Ku M, Rose G, Siadecki SD, Saul T. Air and its Sonographic Appearance: Understanding the Artifacts. J Emerg Med. 2017 Aug;53(2):241-247. doi: 10.1016/j.jemermed.2017.01.054. Epub 2017 Mar 31. PMID: 28372830.

Tuesday Advanced Cases & Procedure Pearls

Traumatic Oculocardiac Reflex by Dr. Tara Ferrante and Dr. Simon Sarkisian

Case: A 12-year-old male was hit in the right eye with a baseball just prior to arrival, now with headache, nausea, and vomiting, with swelling and pain around his right eye.  Patient was unable to look upward, and had pain with looking downward. When he presented to the Emergency Department, his initial heart rate was 44 BPM. Patient received emergent CT head which showed small volume retrobulbar hematoma, concern for entrapment of the right lateral rectus muscle, and acute mildly displaced right orbital floor fracture. Ophthalmology and OMFS were emergently consulted and recommended transfer for pediatric oculoplastic evaluation for retrobulbar hematoma, right orbital floor fracture, and high concern for entrapment.

Pearls:

  • A drop in heart rate by more than 20%, with associated nausea, syncope, or hypotension, after force is exerted on the extraocular muscles or globe of the eye, is known as the oculocardiac reflex. The bradycardia that develops is typically sinus bradycardia. In some cases, this reflex has been known to cause arrhythmias, asystole, and cardiac arrest.  This reflex can occur with facial trauma and nerve blocks, however, it is most commonly found during ophthalmologic surgery.
  • This reflex occurs with activation of the vagus nerve from nerve pathways originating from the stimulation of the opthalmic division of the trigeminal nerve.  The vagus nerve activation results in a diminished chronotropy, creating the response.

Treatment:

  • Removal of the cause, which in the setting of trauma, means consulting ophthalmology for an intervening procedure.
  • In the interim, patients can be stabilized using management for bradycardia, such as atropine, placing the patient on the pacing pads, and careful cardiac monitoring. 
  • If signs and symptoms are concerning for oculocardiac reflex in the setting of trauma, emergent CT and ophthalmology consult is recommended.  Evidence of ocular muscle entrapment, such as limited extra-ocular movements, diplopia, or proptosis, is an indication for emergent ophthalmology consult.

References:

1. Cavuoto, K, Barmettler, A, Prakalapakorn, G, Yen, M, Puente, M. Oculacardiac Reflex. EyeWiki from American Academiy of Opthalmology. March 30, 2023. https://eyewiki.aao.org/Oculocardiac_Reflex.

2. Dunville LM, Sood G, Kramer J. Oculocardiac Reflex. [Updated 2022 Sep 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499832/

3. Sires BS, Stanley RB Jr, Levine LM. Oculocardiac reflex caused by orbital floor trapdoor fracture: an indication for urgent repair. Arch Ophthalmol. 1998;116(7):955-956.

4. Walker RA, Adhikari S. Eye Emergencies. 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. Accessed September 16, 2023. https://accessemergencymedicine-mhmedical-com.ezproxy.rowan.edu/content.aspx?bookid=2353&sectionid=222404436

Friday Board Review

Board Review with Dr. Alex Hilbmann

A 28 year old female G4P2 at 8 weeks gestation presents to the Emergency Department after vomiting almost four times daily for the past week. She denies any recent fevers, abdominal pain, pelvic pain, or vaginal bleeding. Vital signs include: Temp 37.2 C, HR 105, BP 93/62, SpO2 100%. On exam, she is uncomfortable appearing with dry mucous membranes and intermittently dry heaving into an emesis bag. Blood serum results are pending. Urinalysis reveals 1+ ketones with elevated specific gravity. What is the next best step in management?

A. 0.9% normal saline

B. Prophylactic electrolyte repletion

C. 5% dextrose and 0.9% normal saline

D. Antiemetic and PO challenge

Answer: 5% dextrose and 0.9% normal saline

This pregnant patient is most likely experiencing hyperemesis gravidarum given her presentation of multiple episodes of vomiting, volume depletion, and ketonuria. The treatment for hyperemesis gravidarum includes 5% glucose in IV fluids, anti-emetic drugs, and correction of any electrolyte abnormalities. Nothing should be given by mouth until patient’s nausea is controlled, and although this patient will ultimately benefit from antiemetic administration with the hopes that she will tolerate PO, her signs of volume depletion and ketonuria suggest immediate treatment with 5% dextrose in 0.9% normal saline or lactated ringer solution.

Management of Hyperemesis Gravidarum
First line: pyridoxine (vitamin B6) – pregnancy drug class A
Add on: doxylamine – pregnancy drug class A
Adjuncts: ondansetron, metoclopramide – pregnancy drug class B
IV fluids with dextrose

References:

References: Tintinalli, J., Ma, O., Yealy, D., Meckler, G., Cline, D., Thomas, S. and Stapczynski, J., 2020. Tintinalli’s emergency medicine. 9th ed. [New York]: McGraw-Hill Education, pp.621-622.

Nausea and vomiting of pregnancy. ACOG Practice Bulletin No. 153. American College of Obstetricians and Gynecologists. Obstet Gynecol. 2015; 126(3):e12-24