IDEA Series: Ultrasound-capable, 3D-printed central line trainer

Problem: Central venous line (CVL) placement is a key skill for emergency medicine providers. Sites for central line placement include the internal jugular vein, subclavian vein, and femoral vein. Indications include, but are not limited to fluid resuscitation, medication administration, central venous pressure monitoring, pulmonary artery catheter introduction, and transvenous pacing wire placement. Procedural complications can include catheter-associated infection and arterial puncture. Success rates for CVL placement vary based on location and provider experience [1-3]. Point-of-Care Ultrasound (POCUS) increases both success rate and patient safety when used to guide CVL placement [4].

central line trainer 3d idea

Figure 1. Setup for ultrasound-capable, 3D-printed central line trainer

The Innovation

The ultrasound-capable, 3D-printed central line trainer was created to facilitate realistic training of POCUS-guided CVL placement, specifically utilizing the internal jugular vein. The trainer uses a ballistic gel insert that is ultrasound-capable and replaceable, as needed.

The Learners

The model can be utilized by anyone needing practice and training on central line placement. This includes medical and physician assistant students, residents, and fellows. It will be particularly useful with students familiar with POCUS basics.

Group Size

In our experience, 4-5 students were able to utilize the model before the wear from repeated use began to impact the imaging and structure of the model, necessitating replacement of the insert. The dilation step of the Seldinger technique can be skipped or simulated in order to prolong the life of the gel insert.

Equipment

Description of the Innovation

  • The initial head model was designed using 2 common 3D modeling software systems: Tinkercad and  Meshmixer
  • A generic head and neck model was imported into Meshmixer. Using the available tools in Meshmixer, the head was rotated to the side and the neck was manipulated to enhance the appearance of an extended neck with close attention to the sternocleidomastoid muscle and clavicle.
  • The model was then imported into Tinkercad and a section of the neck was removed, inverted, and manipulated inside of a box to create a negative (mold).

central line trainer tinkercad

Figure 2. Screenshot of head being edited in Tinkercad software

central line trainer tinkercad neck

Figure 3. Screenshot of neck mold being edited in Tinkercad software

  • The head was printed with Polylactic acid (PLA) filament in 2 sections that were then glued together with superglue. The seam was sealed and smoothed with latex caulk. The files for both the head and the mold can be found in this Google Drive folder.
  • A hole was drilled from the base of the neck through the top of the head. A second hole was drilled in the base of the model.
  • To make a suitable tray for the ballistic gel insert, a thin plate was printed and then cut to fit the shape of the neck. Finally, that piece was glued to the bottom of the model.
  • The model was painted using matte spray paint.

central line trainer spray paint

Figure 4. Use of matte spray paint to paint the model

  • The mold was printed next. Two holes were drilled on either side to allow for insertion of latex tubing.
  • The ballistic gel was heated according to the directions on the box. The gel can be colored using dye or acrylic paint. Caution should be practiced when using acrylic paint. The heated gel can foam up, increasing the possibility of injury from burn.
  • While the gel was heating, the mold was prepared. The bottom was coated with a thin layer of dish soap to assist with gel release. Two sections of latex tubing, approximately 2 feet each were inserted into the mold. Modeling clay was used to fill the gaps.
  • Once colored and thoroughly heated, the gel was poured into the mold.

central line trainer mold internal jugular vein

Figure 5. Preparation of the mold in which the heated gel will be poured

central line trainer mold pour

Figure 6. The heated, colored gel is poured into the mold

  • After curing, the latex tubes were removed. The gel neck model was then removed and placed into the accompanying space on the 3d printed trainer.
  • The latex tubing was fished back through the available holes, and filled with water. As an optional step, a 30 cc syringe was attached to one end of the thicker tube. Tube stoppers can also be printed and used in place of hemostats. Pumping the syringe plunger simulates the appearance of arterial flow on ultrasound.

Video Demonstration of Final Product

Lessons learned

We are currently investigating how best to research this model. The model is inexpensive compared to available commercial CVL trainers. We estimate the cost at approximately $80 per model in materials. This, of course, does not include the price of a 3d printer, 18v drill, or drill bit. Two comparable models available for purchase are both listed for over $1000 [5, 6]. The build time is approximately 1 week with time spent printing, glue-drying, and ballistic gel setting. The model can be used repeatedly and the insert remade many times over.

If another model were to be designed, the top of the head could be sacrificed in favor of an elongated neck section. The top of the head provides no value and consumes 3d printing filament. Furthermore, an elongated neck may be preferable for a new learner by allowing more room to practice probe and hand placement.

Theory behind the innovation

Simulation as a means of teaching has been a firmly established practice across the landscape of medical education. The model in question is high-fidelity and offers the user a realistic experience in a low-stress environment. The model is small enough to be portable and can be used with little preparation, making it an ideal tool for just-in-time training in the emergency department.

Tools that allow the learner to practice multiple steps of a skill during one exercise are invaluable for skill development, competency-based medical education and mastery learning.

References

  1. McGee DC, Gould MK. Preventing complications of central venous catheterization. New England Journal of Medicine. 2003;348(12):1123-1133. doi:10.1056/nejmra011883
  2. Schummer W, Köditz JA, Schelenz C, Reinhart K, Sakka SG. Pre-procedure ultrasound increases the success and safety of central venous catheterization. British Journal of Anaesthesia. 2014;113(1):122-129. doi:10.1093/bja/aeu049
  3. E Portalatin M, Fakhoury E, Brancato R, et al. Factors contributing to unsuccessful central line placement in the neck and chest. Surgery: Current Trends and Innovations. 2019;3(2):1-5. doi:10.24966/scti-7284/100015
  4. Saugel B, Scheeren TWL, Teboul J-L. Ultrasound-guided central venous catheter placement: A Structured Review and recommendations for Clinical Practice – Critical Care. BioMed Central. Published August 28, 2017. Accessed September 21, 2022.
  5. Life/form Central Venous Cannulation Simulator. Universal Medical. . Accessed September 21, 2022.
  6. Blue Phantom internal jugular Central Line Ultrasound manikin. 3012495 – Blue Phantom – BPP-060 – Ultrasound Trainers. Accessed September 21, 2022.

SAEM Clinical Images Series: My Eye is Swollen

eye

A 56-year-old male presented to the Emergency Department with a chief complaint of painful eyelid swelling and itching upon waking up. He reported no history of trauma or fever. He had one similar episode in the past which was self-limiting. The patient denied vision loss, diplopia, pain with extraocular movement, and ophthalmoplegia.

Vitals: T 37.4°C; BP 129/73; HR 91; RR 16

General: A/O x 3; well nourished in NAD

HEENT:  Extraocular movements intact in both eyes. Pupils are equal, round, and reactive to light and accommodation bilaterally. Visual Acuity: OD 20/20, OS 20/25.

Left eye: Diffuse swelling and erythema to the left upper and medial lower eyelids with minimal purulent discharge from the lacrimal puncta. Tenderness localized to the medial canthal region.

Right eye: Normal.

Complete blood count (CBC): within normal limits

Comprehensive metabolic panel (CMP): within normal limits

Acute dacryocystitis. Dacryocystitis is defined by inflammation or infection of the nasolacrimal sac. Whether acute or chronic, acquired or congenital, inflammation is caused by obstruction of the nasolacrimal duct usually from infection, trauma, or a space-occupying lesion. The most common infectious organisms are Staphylococcus and beta-hemolytic streptococcus species. The classic clinical presentation is a sudden onset of swelling, erythema, and tenderness in the medial part of the orbit. Conjunctival injection and swelling around the entire orbit can suggest the development of preseptal cellulitis. Complications of dacryocystitis include orbital abscess, orbital cellulitis, vision loss, ophthalmoplegia, and eyelid necrosis. The differential diagnosis includes dacryoadenitis, lacrimal sac or sinonasal tumor, ethmoid sinusitis, and infected sebaceous or dermoid cyst.

Treatment for dacryocystitis depends on the severity and clinical manifestations of the disease. In mild cases, symptoms will resolve with the application of warm compresses, lacrimal sac massage (Crigler technique), and topical antibiotics if indicated. Severe cases may require oral or parenteral antibiotics and surgical decompression.

Take-Home Points

  • Dacryocystitis is inflammation of the medial nasolacrimal sac preceded by obstruction and may be acute or chronic, congenital or acquired.
  • Dacryocystitis exhibits a bimodal age distribution. The common congenital form is found in infancy, and in adulthood at age of 40 years older.
  • Dacryocystitis is occasionally mistaken for dacryoadenitis (inflammation of the nasolacrimal gland with superolateral eyelid edema). Far less common, dacryoadenitis is associated with systemic inflammatory conditions such as malignancy, Sjogren syndrome, sarcoidosis, Crohn’s disease, and other autoimmune diseases.
  • Proper recognition and prompt treatment may prevent serious complications including orbital cellulitis, vision loss, and sepsis.

  • Alsalamah AK, Alkatan HM, Al-Faky YH. Acute dacryocystitis complicated by orbital cellulitis and loss of vision: A case report and review of the literature. Int J Surg Case Rep. 2018;50:130-134. doi: 10.1016/j.ijscr.2018.07.045. Epub 2018 Aug 9. PMID: 30118963; PMCID: PMC6098209.
  • Carlisle RT, Digiovanni J. Differential Diagnosis of the Swollen Red Eyelid. Am Fam Physician. 2015 Jul 15;92(2):106-12. PMID: 26176369.

By |2022-09-11T10:08:30-07:00Sep 19, 2022|HEENT, SAEM Clinical Images|

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.

RegionDateTime
Get Waivered Southeast10/21/202212 PM EST
Get Waivered Northwest11/18/202212 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.

Go to Top