SAEM Clinical Images Series: Unilateral Facial Pain

swelling

A 78-year-old male with a past medical history of Lewy body dementia, hypertension on bisoprolol, hypothyroidism, COPD, chronic lower extremity edema on furosemide, and overactive bladder on oxybutynin presented to the emergency department for evaluation of three days of progressively worsening left-sided neck and facial swelling. Associated symptoms included poor oral intake, a nonproductive cough, and one week of sore throat.

The black arrow represents the left parotid gland.

Vitals: Afebrile; normal room air saturation

HEENT: Firm, tender, warm and erythematous swelling over the left mandibular ramus that extended to the cheek, left neck, and spread caudally into the supraclavicular region and anterior chest. There were no identifiable hard masses or areas of fluctuance. Further inspection of the oral cavity revealed dry mucous membranes, poor dental hygiene without identifiable dental abscess, tonsils were normal size and equal bilaterally, and uvula was midline. Direct pressure externally over the area of concern revealed purulent discharge from Stenson’s duct.

White blood cell (WBC) count: 22.15

Comprehensive metabolic panel (CMP): Na 131; BUN 39; Cr 3.3

Lactic acid: 2.9

Acute suppurative parotitis (ASP) is a serious bacterial infection of the parotid gland that occurs in patients with diminished salivary flow, increased susceptibility to infection, and poor oral hygiene. Our patient had multiple risk factors for this disease which can include dehydration, advanced age, sialolithiasis, medications (diuretics, beta-blockers, antihistamines, phenothiazines, tricyclic antidepressants, anticholinergics), and certain disorders including diabetes, HIV, hypothyroidism, Sjogren’s syndrome. The most common organisms responsible for ASP are Staphylococcus aureus and oral flora anaerobes.

The most feared complications include supraglottitis, cervical necrotizing fasciitis, and other deep neck space infections which can be surgical emergencies and rarely cause impending airway obstruction. Further central and vascular complications include brain abscess, central venous thrombosis, and Lemierre’s syndrome

Take-Home Points

  • The role of bedside ultrasound in acute suppurative parotitis can help to rule out a superficial abscess or sialolithiasis. CT scan is beneficial in ruling out deep space infections as a complication from this disease process or other causes of head and neck swelling.
  • ASP-associated complications are rare but can lead to significant morbidity and mortality secondary to the parotid gland’s proximity to vital structures and ability to spread to adjacent deep spaces.
  • Emergency medicine physicians will manage acute suppurative parotitis and must be aware of the potential complications when determining safe disposition and appropriate treatment.

  • Markovich A, Ronen O. Factors predicting length of stay in patients hospitalized for acute parotitis. J Investig Med. 2021 Feb;69(2):388-392. doi: 10.1136/jim-2020-001506. Epub 2020 Oct 21. PMID: 33087427.

By |2022-09-11T10:03:16-07:00Sep 12, 2022|HEENT, SAEM Clinical Images|

SAEM Clinical Images Series: Breast Swelling

A female in her 50s with a past medical history of coronary artery disease, pacemaker placement, hypertension, and ESRD presented to the emergency department with the chief complaint of missed dialysis, breast engorgement, and an increase in vascularity in her chest and abdomen. The patient reported an increase in breast swelling and increased vascularity in her belly over the past three months. Additionally, she woke up short of breath on the morning of presentation and reported dyspnea at rest. She denied chest pain, diaphoresis, breast pain, fever, rash, trauma to the breasts, or drainage.

Vitals: T 36.9°C; HR 105; BP 109/74; RR 20; O2 sat 97% on nasal canula @ 3L

Neck: JVD

Lungs: Bilateral crackles

Chest and abdomen: Increased vascularity

Breast: Bilateral breast swelling and redness

Lower extremity: Bilateral pitting edema and varicose veins

Basic metabolic panel (BMP): K 6.9; Cr 9.53

Brain natriuretic peptide (BNP): >35,000

Troponin I: 0.1

DDX: Inflammatory carcinoma, mastitis, superior vena cava syndrome, portal hypertension, pulmonary hypertension, pulmonary embolism.

Superior vena cava (SVC) syndrome results from any condition that leads to obstruction of blood flow through the SVC. Our case was caused by complete occlusion from a thrombus and the patient presented with bilateral breast swelling, skin changes (peau d’orange), and an increase in vascularity in the abdomen and chest (caput medusa). Breast tissue largely drains into the axillary veins, and more proximally into the subclavian veins. Due to occlusion of the SVC, a complete backup of venous flow occurs, resulting in all of the noted collateral hypervascularity.  Often SVC occlusion is caused by malignancy obstructing the superior vena cava or invading the vein.

The CTA demonstrates occlusion of the superior vena cava. There are multiple varices in the chest wall and the imaged upper abdominal wall. There is also diffuse subcutaneous edema with diffuse soft tissue swelling and skin thickening of the bilateral breasts.

Take-Home Points

  • Consider superior vena cava occlusion in patients undergoing hemodialysis who present with the above physical exam findings.
  • Consider occult malignancy as the source or cause of thrombosis.
  • Be sure to fully expose your patient when appropriate and keep your differential broad.

  • Corduff N, Rozen WM, Taylor GI. The superficial venous drainage of the breast: a clinical study and implications for breast reduction surgery. J Plast Reconstr Aesthet Surg. 2010 May;63(5):809-13. doi: 10.1016/j.bjps.2009.02.055. Epub 2009 Apr 3. PMID: 19345164.
  • Friedman T, Quencer KB, Kishore SA, Winokur RS, Madoff DC. Malignant Venous Obstruction: Superior Vena Cava Syndrome and Beyond. Semin Intervent Radiol. 2017 Dec;34(4):398-408. doi: 10.1055/s-0037-1608863. Epub 2017 Dec 14. PMID: 29249864; PMCID: PMC5730434.

SAEM Clinical Images Series: Localized Weakness

sturge-weber

A 69-year-old Caucasian female with a past medical history of seizures, cerebral vascular accident, and Parkinson’s disease presents by EMS for evaluation of a 30-minute episode of left upper and lower extremity weakness and left facial drooping. The patient complains of a right-sided “migraine-type” headache similar to that experienced with her prior stroke.

Vitals: Temp 36.5°C; BP 186/74; P 74; RR 18; O2 Sat 95%

General: Alert; no acute distress

Skin: Warm; dry; dark red discoloration localized to the left side of face, neck, chest, and upper extremity

HEENT: Normocephalic; left-sided facial droop; pupils are equal round and reactive to light

Cardiovascular: Regular rate and rhythm; no murmurs or gallops

Neurological: Alert and oriented x 4; CN II-XII grossly intact; slow and sluggish speech with left-sided facial droop; motor strength 4/5 LUE and LLE; tremor consistent with Parkinson’s disease

Comprehensive Metabolic Panel (CMP) and Complete Blood Count (CBC) are within normal limits.

Brain Computed Tomography demonstrates chronic atrophy, subcortical calcification, and microvascular ischemia.

Port-wine stain birthmark. This birthmark typically occurs on the forehead, scalp, or around the eye, and is unilateral. It is a manifestation of an overabundance of capillaries near the surface of the skin and exhibits a classic light pink to dark red discoloration.

When located around the eye, port wine stains have been associated with an increased incidence of glaucoma. Large port wine stains on the arm or leg have been associated with extra growth in that limb known as Klippel-Trenaunay syndrome. Port wine staining of the face, forehead, and scalp, when associated with cerebral leptomeningeal angiomas that elicit migraine headaches, seizures, strokes, and intellectual impairment as in this patient, are the classic findings of Sturge-Weber syndrome.

Take-Home Points

  • Sturge-Weber syndrome is the third most prevalent neurocutaneous disorder impacting 1 in 20,000 live births. It is a sporadic congenital neurocutaneous disorder that is caused by somatic activating mutations in the GNAQ gene.
  • Sturge-Weber syndrome is characterized by a facial port-wine stain, leptomeningeal angiomatosis, and glaucoma. Brain involvement can begin early in infancy, and manifests as seizures, strokes, stroke-like episodes, and a variety of neurological impairments.
  • Anticonvulsants, low-dose aspirin, and glaucoma medications are often employed in the management of Sturge-Weber syndrome as well as skin pulse dye laser therapy as desired for cosmesis. The prognosis of this condition depends on the extent of leptomeningeal involvement and the severity of glaucoma.

  • Comi AM. Sturge-Weber syndrome. Handb Clin Neurol. 2015;132:157-68. doi:10.1016/B978-0-444-62702-5.00011-1. PMID: 26564078.
  • Higueros E, Roe E, Granell E, Baselga E. Sturge-Weber Syndrome: A Review. ActasDermosifiliogr. 2017 Jun;108(5):407-417. English, Spanish. doi: 10.1016/j.ad.2016.09.022. Epub2017 Jan 23. PMID: 28126187.

By |2022-08-18T21:54:43-07:00Aug 22, 2022|Dermatology, Neurology, SAEM Clinical Images|

Suboxone and the Emergency Physician: Get Waivered Training

suboxone

Clinical scenario: A 56-year-old male with a past medical history of opioid use disorder presents to the emergency department with acute on chronic right lower flank pain. The patient states the pain was exacerbated while shoveling snow over the weekend and worsens with movement. He feels nauseous but denies any chest pain, shortness of breath, vomiting, abdominal pain, or pain with urination. He denies any history of kidney stones, recent surgeries, and recent injuries. He does not smoke cigarettes, but does drink alcohol almost daily.

His pain actually first started 2 months ago due to a work incident, for which he was prescribed a 1-month supply of hydrocodone for the pain. Although his severe pain reduced in intensity over the first 3 days, he states that he was unable to resist his urge for the painkillers and finished the supply over the next month. The patient was seen in another emergency department one week ago.

On physical exam, the patient seems restless and anxious appearing, but is alert and oriented x 3. His pupils are dilated and reactive to light. His skin is warm and flushed. The patient is tender in the right lower flank region and grimaces upon palpation. The remainder of his exam and vital signs are normal, except for being slightly tachycardic.

Diagnostic testing revealed a normal complete blood count, comprehensive metabolic panel, and non-contrast abdomen/pelvis CT study. His urine toxicology report shows the presence of hydrocodone.

A Tale of 2 Possibilities in Management

Let us assume for a moment that 2 different providers are treating this patient.

  • Physician A treats the patient’s flank pain and nausea in the emergency department, while monitoring him for several hours. Afterwards, the patient is discharged home and instructed to follow up with his primary care physician. After a few days, however, the patient returns with similar symptoms and again with normal lab results and imaging studies.
  • Physician B treats the patient’s flank pain while also recognizing the patient’s opioid dependence by starting the patient on a suboxone treatment plan along with behavioral therapies to curb symptoms of withdrawal and cravings [1]. After a few days, his primary care physician notes that the patient drastically has reduced his dependence on opioids and was on the road to recovery.

Physician B’s approach illustrates the need for physicians to recognize themselves as opioid use disorder (OUD) providers. Part of this role involves understanding and recommending suboxone treatment plans to aid patients in their recovery from opioid addiction.

What is suboxone and why is it important?

Suboxone is a prescription medication that is used to treat opioid addiction in individuals and is composed of buprenorphine and naloxone. Buprenorphine is a drug that blocks opioid receptors and reduces a person’s urges by acting as a partial opioid agonist, while naloxone reverses opioid overdoses. Both components work in conjunction to prevent withdrawal symptoms and thereby helping individuals on the road to recovery. The treatment plan using suboxone is supplemented with a behavioral counseling program to help individuals affected by opioid addiction by targeting the underlying reason for their opioid use and discovering new coping mechanisms [1].

Get X-Waivered to Prescribe Buprenorphine

Based on the Drug Addiction Treatment Act of 2000 (DATA 2000), the DEA-X waiver is a federal regulation that requires physicians to complete training followed by an administrative process in order to have the legal authority to prescribe buprenorphine [2]. Although the research that shows that buprenorphine is effective, only 5% of physicians nationwide are waivered, which limits access to life-saving medications and treatment for patients struggling with opioid addiction [3]. In a 2018 study, researchers demonstrated that 30% of rural Americans are without a buprenorphine provider, compared to the 2% of non-rural Americans [4]. Along with geographical disparities, other health disparities also exist. According to a study published by The Substance Abuse and Mental Health Services Administration (SAMHSA), among minority communities, African American and Latinx populations continue to have significantly lower access to substance-use treatment services [5]. In the wake of the COVID-19 pandemic, it has become increasingly urgent to find innovative ways to help healthcare providers obtain their X-waiver.

2021 Policy Changes

New policy changes under the Biden administration have allowed for expansion of buprenorphine treatment programs for patients with opioid use disorder [6]. As of April 2021, clinicians are now able to complete an exemption form to opt-out of the 8-hour training requirement to obtain the X waiver [2, 6]. Instead, clinicians can now submit a notice of intent form among other documents to SAMHSA that allows clinicians to treat up to 30 patients. When caring for more than 30 patients, X-waiver training is required [2]. Although this a promising start, emergency physicians should continue plans to obtain a DEA-X waiver in order to obtain more formal education, to adjust to any future policy changes, and to treat more than 30 patients. The Get Waivered program offers FREE training courses for healthcare providers to obtain a DEA-X waiver remotely.

Challenges for the Emergency Physician in Managing Opioid Use Disorder

In an emergency department, physicians are often met with several challenges when treating patients with opioid use disorder. These challenges include, but not limited to [7]:

  1. Absent Social Norms (Lack of norms around treating OUD may decrease motivation to obtain the waiver)
  2. Increased Hassle Bias (Irrelevant details make task of completing waiver process more difficult and challenging)
  3. Lack of Salience (Are there any success stories associated with treating patients with OUD with buprenorphine?)

Nudging Physician Behavior

Patients affected by opioid addiction can also be helped by making key changes to physician behaviors. As an example, behavioral researchers at the Nudge Unit at Massachusetts General Hospital recommend using principles of social norming and increasing salience in order to increase the number of physicians that can prescribe buprenorphine [8]. Below are examples that can have lasting effects on how clinicians perceive and approach the opioid epidemic moving forward.

  1. Implement a Get Waivered month at their clinical setting. This establishes a social norm and increases the possibility of more providers obtaining an X-waiver.
  2. Create presentations about the Get Waivered program with detailed instruction on the steps involved in obtaining an X-waiver to minimize hassle bias.
  3. Recruit patients with opioid use disorder to discuss their stories of recovery using buprenorphine during a training session to improve salience [7].

What’s next?

Please register for upcoming FREE training sessions at getwaivered.com/remote to obtain your DEA X-waiver.

Region Date Time
Get Waivered Southeast 10/21/2022 12 PM EST
Get Waivered Northwest 11/18/2022 12 PM EST

Note: The above dates/times are tentative and may be subject to change in the near future.

References

  1. Suboxone.” Addiction Center, 20 Nov. 2020. Accessed May 26, 2022.
  2. Buprenorphine.” SAMHSA. Accessed May 26, 2022.
  3. Berk, Justin. To Help Providers Fight The Opioid Epidemic, ‘X The X Waiver’: Health Affairs Blog. Health Affairs, 5 Mar. 2019. Accessed May 26, 2022.
  4. Andrilla C, Holly A, et al. Geographic Distribution of Providers With a DEA Waiver to Prescribe Buprenorphine for the Treatment of Opioid Use Disorder: A 5‐Year Update. Wiley Online Library, John Wiley & Sons, Ltd, 20 June 2018. Accessed May 26, 2022.
  5. Double Jeopardy: COVID-19 and Behavioral Health Disparities for Black and Latino Communities in the U.S. (Submitted by OBHE) (samhsa.gov). PDF file. Accessed May 26, 2022.
  6. Cornish A. Why new guidelines for opioid treatment are a ‘big deal’. NPR. Published April 27, 2021. Accessed May 26, 2022.
  7. Bruno M and GetWaivered. “Implementation Archives.” Get Waivered.. Accessed May 26, 2022.
  8. Nakagawa J. Nudging ER Doctors To Prevent Opioid Overdoses. Cognoscenti, WBUR, 30 Jan. 2018. Accessed May 26, 2022.
By |2022-08-07T21:56:02-07:00Aug 12, 2022|Public Policy, Tox & Medications|

SAEM Clinical Images Series: Found Down

found down

A 67-year-old caucasian male experiencing homelessness was “found down” in a parking lot. EMS reported that he had a GCS of 6 with a systolic blood pressure in the 80’s, finger stick glucose of 100, and no response to intranasal naloxone. He was intubated in the field and arrived to the emergency department unresponsive with a BP of 95/60, HR 125, T 38°C, and O2 Sat 100%. Hemodynamic stabilization was achieved with central venous access, and laboratory and imaging studies for the evaluation of altered mental status ensued.

General: Disheveled male

HEENT: Normocephalic; PERRLA 3-2 mm; dried blood in nares

Skin: Warm; dry; no visible signs of trauma

Cardiovascular: Tachycardic with no murmurs, rubs, or gallops

Respiratory: Bilateral breath sounds on ventilator; diffuse rales

Gastrointestinal: Soft; non-distended; bowel sounds present

Musculoskeletal: No deformities

Neurologic: Unresponsive; GCS 3

COVID-19 rapid antigen: Detected

Complete Blood Count (CBC): WBC 17 k; Hemoglobin 15; Platelets 185

Comprehensive Metabolic Panel (CMP): Na 133; K 4.6; Cl 91; CO2 21; BUN 18; Cr 2.2; Ca 8.4; Alb 2.1; Tbili 0.4; Alk phos 112; AST 242; ALT 68

ABG on FiO2 100%: 6.99/>95/405/23/100%

Lactate: 16.4

Ammonia: 90

CK total: 716

Trop I HS: 809

PT: 14

INR: 1.05

PTT: 45

Urinalysis: Unremarkable

EtOH, Acetaminophen, Salicylate: Negative

UDS: Negative

Chest Radiograph: Diffuse ground-glass opacities

Air embolism to the right ventricle and pulmonary artery. As little as 20 mL or less of air rapidly infused may cause obstruction, ischemia, and hemodynamic collapse.

Risk factors include central venous catheterization, lung trauma, ventilator usage, hemodialysis, surgery (esp. coronary, neurosurgery), childbirth, and scuba diving barotrauma.

Take-Home Points

  • In the appropriate clinical scenario, especially those involving respiratory, cardiac, and neurologic findings where invasive procedures were utilized, the diagnosis of venous air embolism should be entertained.
  • Immediate management of an air embolism involves administration of 100% oxygen by nonrebreather mask (NRM) or ventilator and placement of the patient in the left lateral decubitus (Durant maneuver) and Trendelenburg positions. Hyperbaric oxygen therapy has also been used if there is no clinical improvement.
  • The purpose of the Durant maneuver and Trendelenburg position is to trap air along the lateral right ventricular wall, preventing right ventricular outflow obstruction and embolization into the pulmonary circulation.

  • Gordy S, Rowell S. Vascular air embolism. International Journal of Critical Illness and Injury Science. 2013;3(1):73. doi:10.4103/2229-5151.109428 Malik N, Claus PL, Illman JE, Kligerman SJ, Moynagh MR, Levin DL, Woodrum DA, Arani A, Arunachalam SP, Araoz PA. Air embolism: diagnosis and management. Future Cardiol. 2017 Jul;13(4):365-378. doi: 10.2217/fca-2017-0015. Epub 2017 Jun 23. PMID: 28644058.

SAEM Clinical Images Series: A Backpacker’s Rash

rash

A 33-year-old female presented with a progressively worsening rash for one week. The patient just finished hiking the John Muir Trail, a backpacking trip that encompassed three weeks and over 240 miles. On the last days of the trip, the patient started to develop a severely itchy, red rash on both feet. She tried using a topical anti-fungal, which seemed to make the rash worse. She now has swelling and difficulty walking. The rash does not involve the hands or other parts of the body. She denies fever, open wounds, nausea, vomiting, or systemic symptoms, and has never had a similar rash before.

Skin: Diffuse edema and erythematous maculopapular rash to both feet, with vesicles and bullae overlying the dorsal and plantar surfaces of toes and feet. No rash proximal to the ankles. No petechiae or purpura noted. Normal hands and palms.

Non-contributory

The rash has both vesicles and bullae which narrow the differential to contact dermatitis and dyshidrotic eczema. Without petechiae or purpura, it is less likely vasculitis (such as exercise-induced vasculitis). There is no fever, spreading redness, or systemic signs, and it is bilateral, making cellulitis less likely. There were no known exposures to poison oak and the patient never walked without shoes or socks. There were no known tick bites, the hike was in California, and the rash did not involve the palms, making an infectious cause such as Rocky Mountain Spotted Fever unlikely. The rash became worse with topical anti-fungal cream, making fungal infection less likely.

The most concentrated areas of the rash are on the plantar surface of the foot and toes. Upon further inspection, it appears in a pattern that may be consistent with sports tape being used during hiking for blisters and plantar fasciitis pain. The patient later received patch testing by dermatology and was diagnosed with a colophony allergy. In this case, colophony was found in the sports tape causing severe allergic contact dermatitis on the feet. This is a T-cell-mediated reaction caused by repeated exposure to an allergen on the skin. Colophony is a mixture of many different compounds that are all derived from pine trees and is a common ingredient in medical and sports tapes. It is also sometimes used in making shoes.

Take-Home Points

  • The presence of vesicles and bullae narrow differential to contact dermatitis or dyshidrotic eczema. Both of these should respond to topical and/or oral steroids.
  • Look for patterns on the highest concentrated area of the rash to suggest allergic contact dermatitis.
  • Repeated lengthy exposure over a short course of time can cause allergic contact dermatitis to develop.

  • Litchman G, Nair PA, Atwater AR, Bhutta BS. Contact Dermatitis. 2022 May 8. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan–. PMID: 29083649.

Trick of the Trade: Getting the last bit of ultrasound gel from the bottle

It’s a busy shift and you need to perform a bedside ultrasound on a patient’s belly to rule out cholecystitis, when you realize that the ultrasound gel bottle is nearly empty. No matter how many times you vigorously shake the bottle, it’s impossible to get the viscous gel out. In a pinch, you could use hand sanitizer, sterile lubricant, or even water as a substitute for gel. Or you could run to the storage room on the other side of the busy department to grab a new bottle. Or…

Trick of the Trade

Use centrifugal force to move the gel to the top of the bottle!

trick ultrasound bottle gel out


  • Turn the bottle upside down so the cap is facing the ground.
  • Place the bottle into a (fresh) patient’s sock or transducer cover. Alternatively, you can use a plastic bag or ortho tubular stockinette.
  • Firmly holding the bag, and spin the bag for a few seconds in a circular motion, almost like you were throwing a grappling hook.
  • The centrifugal motion will generate an outward force pushing all of the viscous gel to the bottle cap!
  • Once you’ve used the gel, store the bottle cap-side down so you don’t have to do this again.

This trick is useful in a pinch, because it makes use of the entire gel bottle and promotes an eco-friendly use of ED resources.

Tip: Just don’t let go while you swing, lest you turn that patient with the belly pain into a trauma activation from a bottle to the face.

Interest in other tricks?

Read more articles in the Tricks of the Trade series.

By |2022-07-25T11:26:09-07:00Jul 27, 2022|Tricks of the Trade, Ultrasound|
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