EM Quick Hits 28 Cardiogenic Shock, Radiation Dose in Pregnancy, PoCUS in Airway Management, VIPIT, Angiotensin II, Short-Term Steroid Safety

Topics in this EM Quick Hits podcast

Anand Swaminathan on an approach to cardiogenic shock (0:53)

Hania Bielawska on myths of radiation dose in pregnant patients (8:55)

Hans Rosenberg & Michael Gottlieb on the value of point-of-care ultrasound for airway management (14:46)

Menaka Pai on Vaccine-Induced Prothrombotic Immune Thrombocytopenia (VIPIT) following AstraZeneca COVID-19 vaccination (21:31)

Brit Long & Michael Gottlieb on angiotensin II vasopressor for distributive shock – is it ready for prime time? (30:45)

Michael Schull on safety of short-term steroid use – a critical appraisal (36:11)

Podcast: Play in new window | Download (Duration: 48:17 — 44.3MB)

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Podcast production, editing and sound design by Anton Helman

Podcast content, written summary & blog post by Brit Long, Raymond Cho & Anton Helman

Cite this podcast as: Helman, A. Swaminathan, A. Rosenberg, H. Gottlieb, M. Pai, M. Long, B. Schull, M. EM Quick Hits 28 – Cardiogenic Shock, Radiation Dose in Pregnancy, PoCUS in Airway Management, VIPIT, Angiotensin II, Short-Term Steroid Use. Emergency Medicine Cases. May, 2021. https://emergencymedicinecases.com/em-quick-hits-may-2021/. Accessed [date].

An Approach to Cardiogenic Shock

1.Identify cardiogenic shock

• Physical exam findings including altered mental status, cool skin and hypotension are nonspecific
• POCUS via RUSH or HI MAP protocol, and ECG can rapidly identify patients in cardiogenic shock

2. Identify the cause of cardiogenic shock to guide management

• Dysrhythmia (i.e. ventricular tachycardia)
• Valvulopathy – POCUS may identify acute regurgitation, aortic lesion or blown valve and if identified, cardiothoracic surgery should be consulted emergently
• Ischemia
  • Patients in cardiogenic shock secondary to ischemia ultimately require angioplasty or thrombolysis; however, these patients require hemodynamic support while awaiting definitive care in the ED
  • Patients in cardiogenic shock are acidemic and hypoxic, and require resuscitation before intubation; non-invasive PPV and high flow nasal cannula may be used to improve myocardial oxygen delivery and prevent intubation
  • Patients with evidence of end-organ hypoperfusion require vasopressor support, with the goal to increase myocardial perfusion while minimizing the increase in myocardial demand; consider norepinephrine and epinephrine as first-line agents at the minimal required dose to restore end-organ perfusion
  • As blood pressure rises, repeat cardiac POCUS to assess for improvements in contractility; no further intervention is necessary if improved, but consider starting dobutamine if contractility remains inadequate
  • If available in your facility or nearby transfer, consider speaking with intensivist about ECMO, LVAD or Impella device

Myths of Radiation Dose in Pregnant Patients

• Maternal illness in pregnancy is common and frequently requires radiographic imaging, but confusion about the safety of radiation often results in avoidance of essential diagnostic imaging
• It would take ≥ 50 mGy of radiation to harm fetus in any way at any stage of development
• Fetal radiation doses
  • Extremity X-ray: 0.001 mGy
  • C-spine X-ray: 0.001 mGy
  • Chest X-ray: 0.01 mGy
  • CT head/neck: 01 mGy
  • CT abdomen (low dose protocol): 1.4 mGy
  • CT pulmonary angiogram: 0.01-0.66 mGy
  • VQ Scan: 0.01-0.5 mGy

Bottom Line: appropriate imaging should not be withheld from pregnant patients due to fears of fetal radiation exposure. The potential harms of missed or delayed diagnosis is often far more dangerous than the imaging study in question. Speak to your radiologist about options for low dose CT protocols.

More on radiation dose in pregnancy:

Unity Health plain language guide on imaging in pregnancy

ACOG guidelines for diagnostic imaging during pregnancy and lactation

Point-of-Care Ultrasound in Airway Management – ETT Position Confirmation, Landmarking for Cric, Difficult Airway Assessment

POCUS in the confirmation of endotracheal intubation

• In cardiac arrest, capnography is only 60-88% sensitive for confirmation of endotracheal intubation. PoCUS is 98.7% sensitive and 97.1% specific for confirmation of endotracheal intubation, and can rapidly confirm tube placement in a mean of 13.0 seconds
• Technique
  • Place linear probe transversely on the suprasternal notch
  • Trachea is located midline behind the thyroid gland appearing as a hyperechoic circular structure
  • Static method: look for the presence of a tube in the trachea and laterally at the esophagus for possible incorrect tube placement. The esophagus normally appears small and deflated but may appear as a smaller circle lateral to the trachea if the tube is incorrectly placed. Twisting the tube can also show motion artifact where the tube is present.
  • Dynamic technique: watch the tube pass through the cords in real time; there will be a flutter of activity as it passes through the vocal cord. Disadvantages include making difficult intubations even more challenging and being difficult to perform with a single provider.

Orientation of probe for transtracheal ultrasound (source: CJEM)

(a) Tracheal Intubation (b) Esophageal Intubation (source: CJEM)

POCUS in landmarking for cricothyroidotomy

• POCUS has been shown to be superior to the landmark technique and can be performed in under 30 seconds
• Technique
  • Place the probe transversely across the cricoid cartilage and identify the thyroid cartilage superiorly (hyperechoic triangular structure). Move caudally to visualize the cricoid membrane (large circular ring followed by a series of smaller rings inferiorly). The cricothyroid membrane is just above, appearing as a hyperechoic white line with distal reverberation artifact. Identify important structures around this and mark the skin.

Cricothyroid membrane (arrow) in transverse (a) and longitudinal plane (b) (source: CJEM)

POCUS in difficult airway assessment

• In patients with stridor, POCUS allows visualization of a mass or subglottic pathology that will make intubation more challenging
• In children and adults who have been intubated before, POCUS allows visualization of subglottic stenosis that may be difficult to predict externally

Videos on POCUS in airway management:

P2SK Airway Assessment Using POCUS

InterAnest POCUS for surgical airway

Vaccine-Induced Prothrombotic Immune Thrombocytopenia (VIPIT) Following AstraZeneca COVID-19 Vaccination

Decision Tree for Diagnosing and Ruling out VIPIT (Source: Science Briefs of the Ontario COVID-19 Science Advisory)

Background

• VIPIT is a rare phenomenon (1 in 125,000-1,000,000) originally reported in Europe in patients who received the AstraZeneca (AZ) COVID-19 vaccine
• The AZ vaccine may trigger an immune response that attacks platelets to create a prothrombotic state, and result in arterial and venous clots as well as DIC and thrombocytopenia
• VIPIT is managed differently from other clots and carries a high mortality (~40%) and is therefore, essential to rapidly diagnose and manage

Clinical assessment

• Patients present 4-20 days after vaccination with features that correspond to clots in different sites
  • Cerebral sinus vein thrombosis: persistent, severe headache, focal neurologic deficits, or seizures
  • Pulmonary embolism: dyspnea, chest pain
  • Splanchnic thrombosis: abdominal pain
  • Limb ischemia/DVT: erythema and swelling or pallor and coldness

Investigations

• CBC (VIPIT is unlikely if platelet is above 150 x 10^9/L)
• An elevated d-dimer, normal blood film and thrombosis on imaging presenting 4-20 days after the AZ vaccination establishes a presumptive diagnosis of VIPIT
• Call hematology for confirmatory diagnosis with heparin-induced thrombocytopenia (HIT) testing and assistance in management

Management

• No heparin or platelet transfusions
• Initiate direct oral anti-Xa inhibitors (DOAC) e.g., rivaroxaban, apixaban or edoxaban
• IVIG 1 g/kg for at least 2 days in severe or life-threatening thrombosis

Angiotensin II Vasopressor for Distributive Shock – Is it Ready for Prime Time?

Mechanism: Angiotensin II can cause smooth muscle contraction, activation of the sympathetic system, and salt and water reabsorption, resulting in increased MAP and circulating volume

Studies: ATHOS-3 found improved MAP in patients receiving angiotensin II (70% vs. 23%), as well as reduced norepinephrine; several post hoc analyses based on subgroups found angiotensin II may reduce mortality, but these were critically ill patients, and studies were industry sponsored; patients with burns, liver failure, cardiac arrest, myocardial infarction, and neutropenia have been excluded from studies

Side effects: Risks include an increase in venous thromboembolic events (VTE), and currently the FDA recommends VTE prophylaxis for patients receiving angiotensin II; some patients may have a hypertensive response to angiotensin II, so close monitoring is recommended

Dosing: Angiotensin II time of onset is 60 s, and the half-life is 30 s; current guidelines suggest starting at an initial dose of 20 ng/kg/min IV and titrating every 5 min in increments of 15 ng/kg/min, with a max dose in the first 3 hours of 80 ng/kg/min and 40 ng/kg/min thereafter

Bottom Line: While angiotensin II is FDA approved for distributive shock, many questions remain; it may be effective for those with refractory hypotension, but more study is needed

Safety of Short-Term Steroid Use – A Critical Appraisal

Design: nationwide population-based cohort study in Taiwan that was performed as a self-controlled case series (i.e., patients served as their own controls). 15,859,129 patients were enrolled and 2,623,327 of them received a single steroid burst (<= 14 days). The objective was to examine the association between short-term steroid burst and adverse events, specifically GI bleeding, sepsis and heart failure; this was done by comparing risk of developing these adverse effects prior to receiving steroids, to their risk in the month after receiving steroids.

Outcome: incidence of GI bleeding, sepsis, and heart failure.

Results: incidence rates per 1000 person-years for patients who received steroid bursts were 27.1 (95% CI, 26.7 to 27.5) for GI bleed, 1.5 (95% CI, 1.4 to 1.6) for sepsis and 1.3 (95% CI, 1.2 to 1.4) for heart failure. There was a 1.8 to 2.4-fold increased risk for GI bleed, sepsis and heart failure in the first month after steroid burst.

Problems with this study: in the ED, patients are put on steroids for a few days rather than an entire year. If converted to risk per person-weeks, the absolute risk of GI bleed in those who received steroids is 0.05% per week while those who did not was 0.03% per week (absolute risk difference of 0.02% but relative risk difference of 80%). The risk of sepsis in patients who received steroids was 0.003% per week while those who did not was 0.002% per week. This difference was even smaller in heart failure. The absolute risk is very small but relative risk is significant given the large population studied.

Conclusion: relative risk of adverse effects after short courses of steroids is large but absolute risk difference is comparatively small.

Bottom Line: the benefits of a short course of steroids in most cases outweigh the risk of adverse events. Consider both absolute and relative risk when evaluating these studies.

None of the authors have any conflicts of interest to declare