Friday Board Review

Board Review by Dr. Edward Guo (Edited by Dr. Parikh)

A postpartum 34 year old female with a past medical history of hypertension presents for shortness of breath. Symptoms have been progressive over one month. She called EMS today when she was too short of breath to walk up one flight of stairs to care for her 13 week old infant. She denies fever, cough, chest pain, or recent illness and is not taking any oral contraceptives. Vital signs include Temp 99.0F, HR 96, BP 170/90, RR 22, SpO2 95% on room air. On exam, she has conversational dyspnea with no increased work of breathing. There are rales at the bilateral lung bases and 2+ pitting edema of the bilateral lower extremities. A bedside echocardiogram is notable for a dilated left ventricle with reduced ejection fraction. Which of the following is the most likely etiology of her symptoms? 

A: Cardiac infiltrative disease

B: Coronary artery atherosclerosis

C: Venous thromboembolism

D: None of the above

Answer: None of the above

This patient is likely presenting with peripartum cardiomyopathy, a rare but potentially fatal complication of pregnancy. The cause is unknown and most commonly occurs in the last month of gestation or within 5 months of delivery. The presenting symptoms and overall management of the condition are similar to other causes of congestive heart failure. Most patients will recover normal ejection fraction within the first 6 months of delivery. Ventricular dysrhythmias caused by persistent dilated cardiomyopathy may warrant an implantable defibrillator-pacemaker.

Cardiac infiltrative diseases such as amyloidosis or sarcoidosis most commonly cause diastolic dysfunction, not systolic dysfunction. Coronary artery disease is the most common cause of congestive heart failure but is unlikely in a 34 year old with minimal risk factors. A pulmonary embolism would cause right heart failure, not left ventricular systolic dysfunction.

 

Peripartum Cardiomyopathy
Most commonly occurs in last month of pregnancy or within 5 months of delivery
Dilated cardiomyopathy without previous heart disease
Treat similarly to other causes of congestive heart failure
Majority of patients recover normal ejection fraction

References:

Young JS. Maternal Emergencies After 20 Weeks of Pregnancy and in the Peripartum Period. 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 Education; 2020.

Arany Z, Elkayam U. Peripartum Cardiomyopathy. Circulation. 2016 Apr 5;133(14):1397-409. doi: 10.1161/CIRCULATIONAHA.115.020491. PMID: 27045128.

“Peripartum Cardiomyopathy – Summary 1. Definition …” GrepMed, 16 Sept. 2020, www.grepmed.com/images/10231/peripartum-treatment-diagnosis-management-cardiomyopathy. Accessed 4 Apr. 2024.

Thursday Conference Content

From the archives: Trigger points for pain control with Dr. Christine Collins

Question: Do trigger point injections with lidocaine lead to lowering pain for patients with point tenderness in their neck or back when compared to standard therapies?

Clinical Importance? Musculoskeletal neck and back pain can pose a challenge to treat when patients do not respond to NSAIDs or have a contraindication to NSAID use, and trigger point injections pose a solution to this. 

Yanuck et al: This is a single blind, prospective, randomized trial conducted at a single level I academic Emergency Department (n=62) with the goal to assess whether trigger point injection with 1% lidocaine results in decreased pain scores when compared to conventional therapy in the treatment of myofascial pain syndrome of the neck/back. For the primary outcome, the mean difference in NRS score when comparing trigger point to control was reported as a statistically significant different (ANCOVA, F[1,50]=25.97, p<0.001). The length of ED stay was also statistically lower in the trigger point injection group. Finally, trigger point injection patient received less opioid prescriptions compared to standard therapy. 

Limitations:  not double blinded, study personnel were in room with treating physician while doing injections, variability in competence of treating physicians, no sample size calculated before the study was done, loss of study participants/drop-outs (especially in the control arm), no tests run for normality of data, pain scores reported as means (outliers can significantly affect), “standard therapies” were broad and not clearly discussed or reported, significant amount of opioid prescriptions, convenience sampling limiting generalizability, 20 minute timeline may have favored injections over other therapies, no follow up period after ED, did not discuss adverse events or side effects reported   

Kocak et. al: This is a randomized prospective study (n=80) at a single Emergency Department which aimed to compare trigger point injections with 2% lidocaine to IV NSAID (dexketoprofen) in the treatment of lower back pain.The study found a statistically significant difference in pain scores reported by the trigger point injection group and the NSAID group (mean pain score trigger point: 7.55, NSAID 7.22, p<0.05), with a significantly higher response to treatment recorded in the trigger point group, with 21 out of 22 responding to trigger points and only 20 out of 32 responding to NSAIDs (p=0.008)

Limitations: Not blinded, no longer term follow up, no conclusions can be made about side effects/adverse effects, no definition of “experienced and trained professionals”

  • Although both studies supported that trigger point injections can reduce pain, both were limited. They did not follow up long enough to suggest a duration of therapeutic effect or address adverse effects adequately. Both studies also did not describe in detail a standardized training process for providers performing the injections. 
  • Trigger point injections are a promising treatment for musculoskeletal pain, however based on my review of the literature, I would not routinely use trigger point injections to treat musculoskeletal back or neck pain. More research should be dedicated to address the length of time the therapy lasts as well as adverse effects that are possible.
  1. Yanuck, Justin, et al. “Pragmatic Randomized Controlled Pilot Trial on Trigger Point Injections with 1% Lidocaine versus Conventional Approaches for Myofascial Pain in the Emergency Department.” The Journal of Emergency Medicine, vol. 59, no. 3, 2020, pp. 364–370., https://doi.org/10.1016/j.jemermed.2020.06.015. 
  2. Kocak AO, Ahiskalioglu A, Sengun E, Gur STA, Akbas I. Comparison of intravenous NSAIDs and trigger point injection for low back pain in ED: A prospective randomized study. Am J Emerg Med. 2019 Oct;37(10):1927-1931. doi: 10.1016/j.ajem.2019.01.015. Epub 2019 Jan 15. PMID: 30660342.
Wednesday Image Review

What’s the Diagnosis? By Dr. Edward Guo

A 50 year old male with a past medical history of Crohn disease with ileocolectomy presents via EMS for shortness of breath. Prior to arrival to ED, patient was found to be hypoxic and in acute respiratory distress prompting rapid sequence intubation by EMS. Vital signs are notable for hypotension and tachycardia. On exam, there are equal breath sounds bilaterally. His abdomen is distended with bruising on the left flank. GCS is 3T. A portable chest x-ray is obtained to confirm endotracheal tube placement and is shown below. What’s the diagnosis?

Answer: Pneumoperitoneum

  • Most commonly caused by gastrointestinal perforation from etiologies such as peptic ulcer disease, traumatic injury, bowel obstruction, or infection.
  • While CT is the gold standard for diagnosis, a chest x-ray may be utilized to quickly assess for presence of subdiaphragmatic air.
    • Sensitivity of upright chest x-ray to detect pneumoperitoenum varies across studies but is up to 80%.
    • Upright positioning for 10 minutes prior to radiograph or lateral upright positioning may increase sensitivity to over 90%.
    • Specificity is approximately 90%.
  • Management includes emergent surgical consultation, broad spectrum antibiotics with anaerobic coverage, and gastric decompression.

References:

Bogle AM, Gratton MC. Peptic Ulcer Disease and Gastritis. 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 Education; 2020.

Stapakis JC, Thickman D. Diagnosis of pneumoperitoneum: abdominal CT vs. upright chest film. J Comput Assist Tomogr 1992;16:713–16.

Woodring JH, Heiser MJ. Detection of pneumoperitoneum on chest radiographs: comparison of upright lateral and posteroanterior projections. Am J Roentgenol 1995;165:45–7.

Tuesday Advanced Cases

Critical Cases – Compartment Syndrome!

by Carlos Cevallos M.D.

Case:

A 60 year old male with a PMH of DM, HTN, HLD, MI presents to the ED after being found down with waxing and waning mentation. The patient complains of abdominal pain and diffuse myalgias.

BP 76/56, HR 92, Temp 98.4F, RR 22. 

Physical exam

Pressure wounds of the right rib cage, right side of his forehead

Right calf tenderness with a firm anterior compartment, cool/pale right lower extremity, dorsalis pedis and posterior tibial pulses were unable to be palpated.

ECG:

ECG interpretation: Peaked T waves, widened QRS concerning for hyperkalemia

Clinical course:

1L bolus of LR

IV calcium gluconate for possible hyperkalemia

Surgery was immediately consulted due to concern for compartment syndrome

Labs were notable for a potassium of 7.2, creatinine of 3.49, creatinine kinase of 188,760, a lactate of 4.0, and ALT/AST in the 3,000s/5,000s

Given intermittent hemodynamic instability a dialysis line was placed for definitive hyperkalemia management

Patient underwent emergent lower extremity fasciotomy with surgery

Compartment syndrome learning points:

·       Diagnosis is both clinical and by compartment pressure measurements

·       Compartment pressure >30mmHg or a delta pressure <30mmHg (diastolic BP – compartment pressure) is diagnostic

·       Clinical findings: 6Ps. Pain is the earliest and often only symptom, the rest are late findings.

o   Pain out of proportion to the exam (most common finding)

o   Pallor

o   Paresthesia

o   Paresis/paralysis

o   Pulselessness

o   Poikilothermia

·       Management: Immediate surgical consult for fasciotomy

Friday Board Review

Board Review by Dr. Vidhi Parikh

43-year-old with woman with history of insulin dependent diabetes and HTN who presents with vision loss of her L eye. Patient states 1 day prior she initially had blurred vision, followed by sudden vision loss 2 hours after the onset of symptoms. Patient with a frontal headache but denies any weakness or numbness. Vitals are as follows: BP- 145/90; HR- 98; T- 98.7; SpO2- 98% on RA; RR- 17. Visual acuity: 20/60 on the R, 20/200 on the L. Patient with intact extra ocular movements and pupils are equal and reactive to light. Fundoscopic exam of the L eye is shown below: 

Acute CRVO

What is the diagnosis? 

  1. Central retinal vein occlusion 
  2. Central retinal artery occlusion 
  3. Bacterial Endocarditis 
  4. Diabetic Retinopathy 
  5. Macular Degeneration 

Answer: A

Patient initially started with blurred vision which then progresses to sudden vision loss which is characteristic of central retinal vein occlusion whereas in central retinal artery occlusion it presents with sudden vision loss. What is pathognomonic on the fundoscopic exam is the blood and thunder appearance. Usually with retinal artery occlusion, a macular cherry red spot is seen. Cotton wool spots are pathognomonic for diabetes/HTN and Roth spots for Endocarditis. 

Central Retinal Artery Occlusion (CRAO) vs Central ...

“Central Retinal Artery Occlusion (CRAO) vs Central …” GrepMed, 1 Oct. 2018, www.grepmed.com/images/3719/centralretinal-management-crao-crvo-ophthalmology.

Diagnosis and management of central retinal vein occlusion. (2020, May 28). American Academy of Ophthalmology. https://www.aao.org/eyenet/article/diagnosis-of-central-retinal-vein-occlusion

Wednesday Image Review

What’s the Diagnosis? By Dr. Katie Selman

A 63 year old female is brought in by EMS after being found down. She has multiple ecchymoses on her chest and bilateral flanks. GCS is 6. After intubation, she is taken for CT head/cervical spine and a CT chest/abdomen/pelvis with contrast. Upon return from CT, x-rays are done (shown below) to further evaluate bruising and a laceration to her L elbow. What’s the diagnosis?

Answer: Contrast extravasation

  • Predisposing factors for contrast extravasation
    • Small IV gauge (22G or less)
    • More distal access (hand)
    • Rapid injection of contrast
  • Incidence: up to 1% of patient receiving IV contrast through peripheral IV
  • Most common symptoms: local pain, swelling
  • Complications occur in < 1 %  (more common with large volume and in patients with atherosclerosis, venous insufficiency, or impaired lymphatic drainage)
    • Compartment syndrome
    • Tissue necrosis
  • Close monitoring required following extravasation
    • Compartment checks, vascular checks, and monitoring of overlying skin
    • Surgery consult for any signs of compartment syndrome or tissue injury
    • Elevate limb, warm compresses may be used
    • Patients rarely require more than conservative supportive treatment

References:

Sbitany, H., Koltz, P. F., Mays, C., Girotto, J. A., & Langstein, H. N. (2010). CT contrast extravasation in the upper extremity: Strategies for management. International Journal of Surgery, 8(5), 384-386. doi:10.1016/j.ijsu.2010.06.002

Sonis, J. D., et al (2018). Implications of iodinated contrast media extravasation in the emergency department. The American Journal of Emergency Medicine, 36(2), 294-296. doi:http://dx.doi.org/10.1016/j.ajem.2017.11.012

Tuesday Advanced Cases

Critical Cases – Hypertensive Emergency!

by Dr. Sarah Perelman M.D.

Today’s case from the EM Daily archives involves one of the rare patients where you DO want to acutely treat elevated blood pressure with intravenous agents….

HPI

  • 48 year old male with PMH HTN presents with blurry vision for 2.5 hours 
  • Patient was using the computer tonight, could not see where the icons were on his desktop, could still see light/colors.
  • He has no pain in his eyes
  • Also reports dyspnea on exertion for 2 days. No headache, no chest pain, no abdominal pain
  • He has not had his anti-hypertensives (he reports he is on 5 different medications) for about 1.5 weeks

Physical Exam

T 98.3 BP 290/120, HR 118, RR 18, SpO2 99%

  • Patient is awake, alert, conversant, appears well and in no distress
  • Neuro: Visual acuity 20/200 OS, OD, OU Normal visual fields Normal pupillary exam Normal extraocular movements Otherwise normal cranial nerve exam Normal strenght in extremities , no pronator drift, normal finger to nose
  • Cardiac: tachycardic, normal S1/S1, no murmurs/rubs/gallops
  • Pulm: clear to auscultation bilaterally
  • Abdomen: soft, nontender, nondistended

Differential Diagnosis 

  • Hypertensive emergency with elevated BP and evidence of end organ damage (decreased visual acuity, evidence of pulmonary edema on bedside US) 
  • Sympathomimetic toxicity (hypertension, tachycardia), though patient reports no ingestions of medications or drugs
  • Thyrotoxicosis 
  • CVA given visual changes, however with no focal visual deficits (no visual field cut, decreased acuity is symmetric bilaterally) 

Initial ED Management 

  • Arterial line place – IV nicardipine started, with goal SBP 210s (25% reduction in the first hour)
  • Bedside lung US performed which demonstrates numerous B lines consistent with evolving pulmonary edema

Labs/Imaging –

  • Hb 6.1, PLT 142, WBC 5.92 – Na 147, K 3.7 – Cr 15.03 (last level in chart 3.95 7 years ago) – HS troponin 223 – pro-BNP 26,930
  • CT Head with 3 small, distinct areas of intraparenchymal hemorrhage

Further Management 

  • Repeat neurologic exam performed and is unchanged
  • Neurosurgery consulted, recommend BP goal under SBP 160
  • Repeat CTH in 4 hours: unchanged 
  • Patient admitted to ICU for IV nicardipine, continuous BP monitoring, and q1 hour neuro checks

Pearls 

  • Hypertensive emergency is acute SBP over 180 with evidence of organ dysfunction
  • Not every patient with SBP over 180 requires emergency BP control
  • In this patient: decreased visual acuity, pulmonary edema, elevated troponin and proBNP, renal failure, and intraparenchymal hemorrhage = hypertensive emergency
  • In managing hypertensive emergency, SBP should not be lowered by more than 25% in the first hour to prevent causing hypoperfusion and cerebral ischemia 
  • Continuous BP monitoring via arterial line is important to carefully titrate medications
  • Nicardepene is an easy to titrate CCB which may be the ideal agent for the treatment of hypertensive emergency
  • Indications for emergent dialysis (AEIOU – acidosis, electrolytes, intoxication, overload, uremia): critical metabolic acidosis, refractory or rapidly increasing hyperkalemia, life threatening intoxication with substance that is able to be removed with HD, volume overload, complications of uremia (pericarditis, neuropathy, encephalopathy)
Monday Back to Basics

Transvenous Pacing

The last two weeks, Dr. Cash taught us about bradycardia and transcutaneous pacing. This week, we dug back years into the archives and pulled out Dr. Pelletier-Bui’s famous post on transvenous pacing.

A timeless classic! Just be sure to know what supplies are available in your department, where to find them, and alternate options if your supplies differ.

References:

Bessman, E. (2019). Emergency cardiac pacing. In Roberts et al (Eds.), Roberts and Hedges’ clinical procedures in emergency medicine and acute care (pp. 288-308).  Elsevier, Inc.

Bohanske. (2013, November 4). Transvenous pacemaker placement – Part I: The walkthrough.  Taming the Sru.  https://www.tamingthesru.com/blog/procedural-education/transvenous-pacemaker-placement-part-1-the-walkthrough 

Mason, J. [EM:RAP Productions] (2018, October 11).  Placing a transvenous pacemaker [Video]. YouTube. https://www.youtube.com/watch?time_continue=24&v=00-T8PcbStE&feature=emb_title