Friday Board Review

Friday Boad Review with Dr. Ethan Anderson

Ethan AndersonLeave a comment

A 65-year-old male presents to the emergency department with complaints of severe shortness of breath and chest pain. He has a history of myocardial infarction and congestive heart failure. On physical exam, he is diaphoretic, hypotensive with a blood pressure of 80/50 mmHg, heart rate of 120 bpm, and jugular venous distension. His lungs reveal crackles bilaterally. An ECG shows ST-segment elevation in the anterior leads, and troponin levels are significantly elevated. Bedside echocardiography reveals an ejection fraction of 25% with global hypokinesis.

Which of the following is the most appropriate immediate treatment?

A) Intravenous fluids bolus
B) Nitroglycerin infusion
C) Norepinephrine infusion
D) Non-invasive positive pressure ventilation

Answer: C) Norepinephrine infusion

Explanation:

This patient is in cardiogenic shock, likely secondary to acute myocardial infarction (AMI) based on his history, clinical presentation, and ECG findings. 

Norepinephrine is widely recommended as a front-line agent for cardiogenic shock. Norepinephrine will improve the blood pressure, but there is a risk that excessive afterload could drop the cardiac output. The cath team should be notified ASAP if MI is the suspected cause of cardiogenic shock. Early consultation of the heart failure team can help guide further management if available at your institution.

Key Points:

  • Cardiogenic shock occurs when there is inadequate tissue perfusion due to the failure of the heart as a pump. It is typically characterized by hypotension, signs of poor perfusion (cold extremities, altered mental status), and pulmonary congestion.
  • The most common cause is an acute myocardial infarction (AMI), leading to severe left ventricular dysfunction. Other causes include Takotsubo, Peripartum Cardiomyopathy, Myocarditis, and Tachymyopathy

Choices:

  • A) Intravenous fluids bolus: Fluid boluses are generally avoided in cardiogenic shock because the failing heart cannot effectively pump the excess fluid, which can worsen pulmonary edema. This patient already shows signs of volume overload (crackles in the lungs and jugular venous distension).
  • B) Nitroglycerin infusion: Although nitroglycerin can reduce preload and improve ischemia in stable patients with myocardial infarction, it is contraindicated in this case due to the patient’s hypotension. Reducing preload or blood pressure further would worsen the shock.
  • C) Norepinephrine infusion: This is the correct answer. In cardiogenic shock, vasopressors such as norepinephrine are used to maintain perfusion by increasing systemic vascular resistance and cardiac output. Norepinephrine is often preferred because it has strong vasoconstrictive effects and some inotropic support, making it suitable for patients in cardiogenic shock with hypotension.
  • D) Non-invasive positive pressure ventilation (NIPPV): While NIPPV can help manage pulmonary edema and improve oxygenation, it does not address the underlying hypotension or poor cardiac output, which are the primary concerns in this case. This may be useful in conjunction with vasopressors but is not the initial definitive treatment for shock.

Takeaway: In patients with cardiogenic shock, the first-line treatment often includes vasopressors, such as norepinephrine, to stabilize blood pressure and ensure adequate organ perfusion while addressing the underlying cause (e.g., revascularization in myocardial infarction).

References:

  • Tintinalli’s Emergency Medicine Manual, 9th Edition
  • Internet Book of Critical Care
Wednesday Image Review

Rib Fractures Part 1: Dr. DeMarzo

Carlos CevallosLeave a comment

Rib fractures can be an incredibly painful condition for patients that is not only painful but also can make breathing difficult and lead to atelectasis and pneumonia. Correct diagnosis of a rib fracture as well as the exact location can help narrow down a differential as well as guide targeted treatments. Diagnosis of fractures can be clinical, but most providers will order imaging. According to the American College of Radiology, in minor blunt trauma that results in only an injury to the ribs, a chest X-ray is rated as “Usually Appropriate” while a rib view radiography is designated a step lower at “May Be Appropriate”. Of note, a rib view radiography is rated as “Usually Appropriate” for any pathologic fractures (i.e Underlying malignancy, metabolic disorders). While useful in identifying secondary injuries such as pneumothorax or flail chest, a chest x-ray can have sensitivities as low as 50% [1]. In the ED CT scans is the standard method through which rib fractures are identified.

A lesser known and utilized diagnostic method is the use of ultrasound, which is becoming more commonly employed in Emergency Departments. While skill level varies and heavily affects results, ultrasound is an effective tool to not only diagnose rib fractures, but also can help deliver a nerve block which provides much needed relief. In fact, in the hands of an experienced provider, ultrasound can be more effective than radiographs; a 2022 meta-analysis of 7 studies with 660 patients demonstrated chest ultrasonography achieving a pooled sensitivity of 89.3% and specificity of 98.4%. [2]

What are we looking for on Ultrasound?

  • A rib fracture is best visualized in a long view of the rib which would be best classified as a transverse view.
  • A fracture is best visualized by tracing the outer edge of the rib to visualize any breaks, bulges, or mismatched ends.
  • The best way to find the fracture: Ask the Patient! Ask them to point to the spot of their worst pain and begin probing there.
  • Some compression given to the probe may identify buckle fractures as seen in Figure 2 below:

Figure 1: Transverse fracture

(Source: https://doi.org/10.1002/sono.12176)

Figure 2: Buckle fracture (visualized w/ compression)

(https://radiopaedia.org/cases/buckle-rib-fracture-on-ultrasound)

Resources:

  1. Bansidhar BJ, Lagares-Garcia JA, Miller SL. Clinical rib fractures: are follow-up chest X-rays a waste of resources?. Am Surg. 2002;68(5):449-453.
  2. Gilbertson J, Pageau P, Ritcey B, et al. Test Characteristics of Chest Ultrasonography for Rib Fractures Following Blunt Chest Trauma: A Systematic Review and Meta-analysis. Ann Emerg Med. 2022;79(6):529-539. doi:10.1016/j.annemergmed.2022.02.006

 

Tuesday Advanced Cases & Procedure Pearls

Advanced Cases: Intramural Aortic Hematoma

Sean CoulsonLeave a comment
By Kane McKenzie, DO

HPI: A 55 year old woman presents to the emergency department for back pain. She reports that while walking she suddenly felt a sharp pain in the center of her back. It feels like stabbing, and is worse with a deep breath or movement. She denies recent trauma. She has a history of hypertension for which she does not take medications. ECG shows NSR with new T wave inversions in lateral leads.


Vitals: BP 230/114 HR 80 RR 20 SaO2 97%


PE: Appears uncomfortable. No murmurs, lungs clear but breath sounds diminished. 3+ Radial and Dorsalis Pedis pulses. Mild tenderness to upper thoracic spine. Neurologic exam is nonfocal.


Labs: High sensitivity troponins 24>24, CBC and BMP unremarkable
Imaging: CTA chest shows intramural hemorrhage of the aortic arch and descending thoracic aorta


Diagnosis: Aortic Intramural hemorrhage – Considered an acute aortic disorder but often differentiated from dissection



Management: 
Similar to aortic dissection. Anti-impulse therapy: HR preferred with Esmolol or Labetolol (HR < 80) , BP (systolic < 120) with Nicardipine or nitroprusside + Emergent surgical consultation


Pathophysiology:
-Hematoma within the medial layer of the aorta without a detectable intimal tear
-Can develop into aortic dissection
-Classified using Stanford or Debakey, same as dissections
-Estimated to account for 5-20% of patients with symptoms consistent with an aortic dissection
-Theorized to occur by either rupture of a penetrating atherosclerotic ulcer or spontaneous rupture of the vasa vasorum
-There is debate whether intramural hematoma should be classified as dissection with thrombosis of the false lumen
-Intimal defects are present in 70% of cases initially diagnosed as intramural hematoma
-Often not able to be identified until surgical repair


References:
Black, James H III. Overview of acute aortic dissection and other acute aortic syndromes. In: UptoDate, Connor RF (Ed), Wolters Kluwer. (Accessed August 16, 2024.)
Tintinalli’s Emergency Medicine 
Gaillard F, Hacking C, Jones J, et al. Aortic intramural hematoma. Reference article, Radiopaedia.org (Accessed on 16 Aug 2024) https://doi.org/10.53347/rID-919

Wednesday Image Review

Abdominal Aortic Ultrasound Review By Dr. Ciervo

Carlos CevallosLeave a comment

 What are we looking for?

  • Aortic Abdominal Aneurysm (AAA) 
  • Aortic Dissection can potentially be seen, but identifying a dissection is not the clinical question when performing an US scan of the aorta

 Which probe do we use?

  • Curvilinear Probe

 How do we find the aorta and identify its vessels?

  • Look for the vertebral body as a landmark! The aorta lies above it in the short axis.
  •  “Seagull Sign” – the hepatic and splenic arteries can be seen in the short axis of the proximal aorta in the epigastric region.
  •  Long axis aorta (sagittal plane) – the Superior Mesenteric Artery (SMA) can be seen rising from the aorta in long axis.
  • “Mantel Clock Sign” – short axis proximal aorta with SMA and splenic vein overlying it superiorly.
  • Iliac Bifurcation- Trace the lower aorta through its bifurcation into the iliac arteries

 What is normal vs. abnormal?

  •  Measure the aorta along it’s course through the abdomen in short axis. > 3 cm from outer edge to outer edge is considered abnormal and concerning for AAA. 
  • Look for dissection flaps and intramural thrombus! 

References:

https://coreem.net/core/abdominal-aortic-ultrasound/ https://www.acep.org/sonoguide/basic/aorta https://radiologykey.com/abdominal-aorta-5/

Tuesday Advanced Cases & Procedure Pearls

Advanced Cases: Stroke in the Sickle Cell Patient

Sean CoulsonLeave a comment

By: Dr. Sean Coulson

HPI: Pt is a 38 y/o male with hx of sickle cell (SS) who presents for generalized headache, facial droop and difficulty speaking. Last known normal was 19 hours PTA. No anticoagulation.

Objective: HR 91, BP 155/91, RR 20, Temp 98F, Accu Check 129 NIH 2 – mild left lower facial droop and mild dysarthria. No other neurologic deficits. Stroke alert is called and CT CTA do not show any acute hemorrhagic infarct or large vessel occlusion. Labs and EKG are sent and the only pertinent result includes a Hb of 6.1 (prior baseline 9).

DDX: acute hemorrhagic / ischemic stroke, seizure, dural venous sinus thrombosis, myasthenia gravis, botulism, complex migraine etc.

Management: Given that this patient was outside of the 4.5 hour window and there was a low suspicion for thromboembolic etiology, TNK was held. In discussion with neurology and hemonc, a shiley dialysis catheter was placed and exchange transfusion was initiated.

Exchange transfusion: Goal is to reduce HbS to < 30% preventing further sickling. In hemorrhagic stroke (primary or secondary to an ischemic stroke), exchange transfusion is still indicated however the goal is to prevent secondary vasospasm and recurrent strokes – data is less clear in terms of overall benefit. If exchange transfusion is not possible, simple regular transfusions are indicated immediately and can act as a bridge until exchange transfusion is established. Hb goal determined in discussion w/ Hematology.

Pearls:

~ Sickle cell is a common cause of acute stroke in children and young adults.

~ SS causes increased risk for cerebral aneurysms and other arterial abnormalities (high risk for carotid dissection, subarachnoid, dural venous thrombosis etc)

~ It is still important in acute strokes to apply general sickle cell crisis management (O2, fluids, pain control, transfusion)

~ Exchange transfusions lower risk of recurrent stroke

~ SS is not an absolute contraindication to TPA

*** Thrombolytics can be given in sickle cell patients if there is a high pretest probability for thromboembolic etiologies of the acute stroke (CAD, PVD, Afib etc) and the patient meets typical inclusion/exclusion criteria. However the benefit of thrombolytics in stroke secondary to sickled RBCs is questionable – data is limited.

~ If exchange transfusion is not possible, discussion w/ hematology and neurology about Hb parameters is paramount.

References

Hulbert ML, Scothorn DJ, Panepinto JA, et al. Exchange blood transfusion compared with simple transfusion for first overt stroke is associated with a lower risk of subsequent stroke: a retrospective cohort study of 137 children with sickle cell anemia. J Pediatr. 2006;149(5):710-712. doi:10.1016/j.jpeds.2006.06.037

Alakbarzade V, Maduakor C, Khan U, Khandanpour N, Rhodes E, Pereira AC. Cerebrovascular disease in sickle cell disease. Pract Neurol. 2023;23(2):131-138. doi:10.1136/pn-2022-003440

Tintinalli J. TINTINALLI’S EMERGENCY MEDICINE : A Comprehensive Study Guide. Mcgraw-Hill Education; 2019:1136.

EM:RAP CorePendium. EM:RAP CorePendium. Published 2024. Accessed August 10, 2024. https://www.emrap.org/corependium/chapter/recZWicqx0K20uwsz/Sickle-Cell-Disease#h.1h9pp1rguxde