Case Conference Summary, August 9, 2017

Case Conference Summary, August 9, 2017

This week in Rapid Fire Case Conference we had a number of great clinical cases and educational pearls.

Dr. Patrick Sylvester presented a case of an elderly gentleman who presented with complaints of fatigue. On arrival he was noted to be hypotensive and diaphoretic. Physical examination revealed JVD and muffled heart sounds. He astutely used bedside ultrasound and saw this:

He astutely recognized physical exam findings of cardiac tamponade (hypotension, JVD, muffled heart sounds, pulsus paradoxus) and ultrasonographic findings.

He subsequently appropriate performed emergent pericardiocentesis, which resolved the patient’s hypotension. A good video to walk you through it. An alternative is to utilize a triple lumen catheter with a spinal needle. Leaving a catheter to allow for continued drainage is certainly a good idea. Temporizing measures to be used include IV fluid administration to maximize preload.

Dr. Jennifer Cotton presented a case of a young patient presenting with dental pain. While the work-up wasn’t specifically discussed, she described use of an inferior alveolar nerve block to help with pain relief. This can be used for numerous purposes to allow for pain relief. To perform the procedure:

  1. Palpate the greatest depth of the anterior border of the mandibular ramus with the index finger or thumb
  2. Pull out the cheek to reveal the pterygotemporal depression (between the raised ridge of mucosa medially and coronoid notch laterally)
  3. Direct the needle from the opposite premolar area and insert into the pterygomandibular depression, 1-1.5 cm above the occlusal plane
  4. Insert until you contact bone (typically 20-25 mm) and withdraw needle a few mm and aspirate to ensure you’re not in a vessel – if no blood then deposit 1.5 mL of bupivicaine

Of course, it’s important to know the complications and ensure the patient understands this is temporary (duration of action of bupivacaine is 120-240 minutes). Complications include:

  • 15-20% failure rate
  • Hematoma
  • Medial pterygoid trismus (delayed presentation ~24 hours, self resolving)
  • Infection
  • Needle breakage
  • Transient facial paralysis from facial nerve block (inappropriate technique)

Dr. Cotton also presented a case of an older male presenting from a long term care facility with concerns of sepsis. On arrival, he was noted to be hypotensive, short of breath, and cool to the touch. She quickly reached for her ultrasound probe and performed a RUSH exam for undifferentiated shock. The exam includes 5 components that can be remembered by the pneumonic “HIMAP” – heart, IVC, Morrison’s pouch (i.e. perform a FAST), aorta, and pulmonary (i.e. lung sliding, B lines, etc.). Her ultrasound revealed findings of a dilated right ventricle, IVC dilation, McConnel’s sign.

She was rightly concerned about PE and discussed the definitions of both submasssive and massive PE:

  • Submassive – systolic blood pressure >90 mmHg but with RV dysfunction or myocardial necrosis
    • RV dysfunction – RV dilation on ECHO/CT, elevated BNP, myocardial necrosis (i.e. elevated troponin) ECG with complete/incomplete RBBB, anteroseptal STE/depression or T wave inversions
  • Massive – systolic blood pressure 15 minutes or causing cardiogenic shock

Dr. Cotton’s patient was in extremis and hypotensive. Given the worsening clinical status with cardiogenic shock, she pushed IV t-PA. After considering contraindications, there are different approaches to dosing described, but is typically given as a 10 mg bolus IV followed by 90 mg infusion over 2 hours. Systemic heparinization is also used and catheter based treatment techniques can be used for patients with a higher risk of bleeding or have submassive PEs. Embolectomy is described as well, but unlikely to be useful in such a crashing patient. For blood pressure support, be cautious with IV fluids! Patients with submassive/massive PEs have acute pulmonary hypertension. Too much fluid can be as bad as too little, leading to further RV dilation and worsening cardiac output. If required for blood pressure support, norepinephrine +/- dobutamine may be considered as well. A good review including contraindications and other management principles.

Taking it a step further, we discussed outcomes of patients with submassive PE regarding long-term follow-up. While treatment with lytics would seem to benefit development of long-term complications, such as chronic pulmonary hypertension, there doesn’t seem to be a huge effect. For a more complete review, go here.

Finally, Dr. Daniel Adams presented some information regarding allergic reactions to local anesthetics and alternatives. Two forms of local anesthetics are typically used: esters (benzocaine, procaine, tetracaine) and amides (bupivicaine, lidocaine, mepivacaine). To remember which drug belongs to what class, you can remember “one eyed ester, two i’s for amides. Regarding allergic reactions, true anaphylactic reactions are rare. More commonly reactions include contact dermatitis or delayed type 4 hypersensitivity reactions from additives and preservatives in the solution. If you are concerned that the patient’s allergy represents anaphylaxis, a medication from the other category can be used (i.e. an amide if the allergy is to an ester and vice versa).

That said, an alternative local anesthetic to the above includes use of SQ benadryl. It works by selectively binding to inactivated sodium channels leading to stabilization of nerve cell membranes and inhibition of downstream depolarization. The duration is described as variable. How do you make it?

  1. Take a vial of 50 mg/mL diphenhydramine
  2. Draw up the entire contents into a 5 cc syringe (total 1 mL)
  3. Dilute this with 4 mL of normal saline (final volume 5 mL)
  4. You are left with a 1% solution (10 mg/mL) of diphenhydramine
    1. Higher concentrations have been associated with skin necrosis

Finally, Dr. Adams presented the case of an older female who presented with fatigue, weakness, insomnia, and intermittent palpitations and tachycardia. She was otherwise well appearing and symptoms had been progressive over the preceding weeks. Review of systems included concerning features for hyperthyroidism and the patient was appropriately worked up and was noted to have an undetectable TSH with an elevated free T4 and free T3. Etiologies of hyperthyroidism were discussed, including Grave, toxic multinodular goiter, thyroid adenomas, and factitious hyperthyroidism. Symptoms are often nonspecific. Severe presentations may include atrial fibrillation, CHF, and altered mental status. Of note, elderly patients may present with depressed mental status, or apathetic hyperthyroidism. A more complete table of interpretation of thyroid hormone levels is listed below. Remember to obtain a free T4 and T3, as only the unbound/circulating fraction is biologically active. Other lab values that might be obtained include a workup for Graves (anti-thyroid receptor antibodies, thyroid stimulating immunoglobulin) and Hashimoto’s.

While hyperthyroidism can represent a spectrum of illness from mild hyperthyroidism to thyroid storm or thyrotoxicosis, sicker patients deserve special attention, including those at risk for impending thyroid storm. The Burch-Wartofsky Point Scale can be used to assess risk. Treatment includes administration of a beta blocker (typically propranolol), methimazole or propylthiouracil, iodine administration, and steroids, as patients are often adrenally insufficient. This is likely best done in conjunction with endocrinology consultation, but rapid identification and management of thyroid storm is highly important.

Acute Chest Syndrome

Authors: Kenneth Akapo, OSU MS4 // Dr. Michael Barrie, OSU EM Attending

A 24 year old female with history of sickle cell disease presents with a 6 hours history of widespread pain. The pain is in her lower back but also present within the lower and upper extremities. She also endorses mild shortness of breath although she attributes this to her pain episode. She mentions being seen a week ago due to a similar episode during which she also had new onset headaches associated with blurry vision. During that episode, CT scan was unremarkable. During the current encounter, there was low concern for ischemic stroke. The headaches have persisted until now, however, she no longer endorses changes in vision. She also denies any other focal neurologic symptoms.

Upon initial examination, the patient appeared to be in mild distress. She was mentating well and exhibited no focal neurologic symptoms.  She was diffusely tender to palpation although she seemed to exhibit more pain when palpating the lower extremities and back. Breath sounds were clear to auscultation bilaterally, and cardiovascular exam was normal.

Before presenting the case to the senior resident, you consider your differential diagnosis – sickle cell pain crisis, acute chest syndrome (ACS), ischemic stroke, acute coronary syndrome (the other ACS), and heart failure among others.

But what findings would help support or refute a diagnosis of acute chest syndrome? And what is the plan to manage the initial diagnosis and treatment of possible acute chest syndrome?

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LEARNing Rounds: Lessons Learned From An Unanticipated Difficult Airway or “Oops, I Need Fresh Underwear!”

Learn, Evaluate, Adopt…Right Now!

Colin G. Kaide, MD, FACEP, FAAEM // Editor Michael G. Barrie MD

LEARN airway word document version of this resource

Case

This patient was an obese male in his 50’s who developed respiratory failure in the ED.  Intubation by a senior resident and a very experienced attending using first GlideScope® (GS) then direct laryngoscopy (DL) were unsuccessful.  They placed a size 5 LMA and were able to successfully oxygenate the patient.  I was called to assist with the airway.  They said they could visualize the cords with DL and with the GS.  They were unable to guide the ETT into position because of what was described as a large amount of “redundant tissue” and some anatomic issue that prevented 2 experienced doctors from guiding the ETT thru the cords.

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Beta Blocker and Calcium Channel Blocker Overdose

Leslie Adrian, MD, OSU EM PGY-1 // Michael Barrie, MD OSU EM

 

You get a call from triage, a 34 year old female is in the waiting room, presenting to ED with chief complaint of intentional ingestion. You briefly examine her; she is well appearing but tearful with a HR of 70 and BP 120/79 and is alert and oriented. She admits to taking thirty of her friend’s blood pressure medication one hour ago, she does not know what it was called, but thinks it ended with an “-olol.” You put her on the monitor, order ingestion labs and then receive a call that a level 1 stroke patient has arrived and needs to be intubated.

15 minutes later, you get a frantic call from the psychiatric nurse stating that your patient’s HR is 30 her blood pressure is 70/40, and she is altered but protecting her airway. You put the patient on oxygen and start fluids immediately, but what do you do next?

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