SAEM Clinical Images Series: There’s a Stone Under My Tongue

stone

A 44-year-old female presented to the emergency department with the complaint of a “stone under [her] tongue.” She reported that the “stone” had been present and painless for two years. The day prior, she began experiencing pain at this site while brushing her teeth. She squeezed the area in an attempt to expel it, but this action only increased her pain.

Vitals: BP 156/92; Pulse 80; Temp 98.4°F; Resp 14; SpO2 100%

General: Sitting on chair, no acute distress

HEENT: Localized swelling to the inferior lingual frenulum at Wharton’s duct with associated erythema. Partially visualized white calculus, palpable through the mucosal membrane.

Sialolith in Wharton’s Duct. There was visual and tactile evidence of a calculus under the patient’s tongue. It had slowly grown and was associated with increased pain and swelling while brushing her teeth.

The majority of sialoliths can be managed conservatively with hydration, moist heat application, massaging of the gland, milking the duct, and advising the patient to suck on tart candies to promote salivation. Larger, more superficial sialoliths may benefit from excision in the emergency department. In the case above, local anesthetic was injected, and manual expulsion was attempted but was unsuccessful. The emergency physician made a single 1 cm incision over the calculus and a 0.5 cm x 0.75 cm sialolith was removed with minimal bleeding. The patient was discharged on a course of amoxicillin-clavulanic acid.

Take-Home Points

  • Dehydration, trauma, anticholinergics, and diuretics predispose to the formation of sialoliths, with 80-90% arising from the submandibular glands. As with our patient, the most common presentation is a single calculus within Wharton’s duct causing pain and swelling during periods of increased salivation.
  • Conservative treatment is the mainstay of sialolith management. Larger, more superficial sialoliths may require excision. Imaging and specialist referral should be considered in cases concerning for tumor, abscess, or treatment failure.
  • Huoh KC, Eisele DW. Etiologic factors in sialolithiasis. Otolaryngol Head Neck Surg. 2011 Dec;145(6):935-9. doi: 10.1177/0194599811415489. Epub 2011 Jul 13. PMID: 21753035.

By |2023-08-27T21:38:49-07:00Aug 28, 2023|HEENT, SAEM Clinical Images|

SAEM Clinical Images Series: A Painful Swollen Digit

finger

A 50-year-old male with a history of polysubstance use disorder and poorly-controlled type 2 diabetes mellitus presents with left hand pain. One week ago, the patient sustained a macerating injury of the left distal middle digit. Since that time he has experienced worsening pain throughout the digit, now associated with diffuse swelling and discoloration. The patient also reports reduction in range of motion.

Vitals: Temp 97.6°F (36.4°C); BP 134/89; HR 87; Resp 16

General: Uncomfortable appearing male.

Musculoskeletal: Left hand third digit with fusiform edema, diffuse erythema, and warmth. Held in passive flexion at rest. Skin breakdown noted at distal fingertip with scant serous drainage. Tender to palpation, most markedly over the volar surface of the PIP joint. Patient reports severe pain with passive extension at the MCP, PIP, and DIP joints.

Glucose: 296

White Blood Cell (WBC) Count: 8,000/μl

ESR: 54 mm/hr

Infectious flexor tenosynovitis is an infection of the flexor tendon and synovial sheath with a significant risk of complications (e.g., tendon rupture, loss of function, amputation) if not promptly treated. Patients classically present 2-4 days after penetrating trauma to the hand (e.g., bite/scratch, puncture wound, laceration, injection).

This diagnosis is suggested clinically by four cardinal findings, the Kanavel signs:

1) diffuse “fusiform” swelling of the digit (most common)

2) digit held in passive flexion

3) tenderness to percussion over the flexor sheath

4) pain with passive extension

Although fundamentally a clinical diagnosis, the initial evaluation for infectious flexor tenosynovitis should include laboratory studies including complete blood count (CBC) and inflammatory markers (ESR/CRP). Radiographs may be performed to evaluate for occult traumatic injury or foreign body. Treatment includes emergent consultation of orthopedics or hand surgery, initiation of intravenous (IV) antibiotics, and hospital admission. Antibiotics should target gram-positive organisms (Staphylococcus, including MRSA, and Streptococcus). In immunocompromised patients, additional coverage against gram-negative organisms and anaerobes may be needed. Risk factors for poor outcomes include immunocompromise (HIV, diabetes, immunosuppression), intravenous drug use, peripheral vascular disease, and polymicrobial infection.

Take-Home Points

  • Infectious flexor tenosynovitis is a surgical emergency that is diagnosed clinically by the presence of one or more of the four Kanavel signs on physical exam.
  • History of trauma or penetrating injury and immunocompromised status should raise suspicion for infectious flexor tenosynovitis; common pathogens include Staphylococcus and Streptococcus species.
  • Treatment includes emergent consultation with orthopedics or hand surgery as well as early initiation of IV antibiotics.

  • Ritter K, Fitch R. Tenosynovitis. In: Knoop KJ, Stack LB, Storrow AB, Thurman R. eds. The Atlas of Emergency Medicine, 5e. McGraw Hill; 2021. Accessed November 30, 2022. https://accessmedicine-mhmedical-com.ezproxy.bu.edu/content.aspx?bookid=2969&sectionid=250459435.
  • Hyatt MT, Bagg MR. Flexor Tenosynovitis. OrthopClin N Am 2017;48:217-27.
  • Pang HN, Teoh LC, Yam AKT, Lee JYL, Puhaindran ME, Tan ABH. Factors affecting the prognosis of pyogenic flexor tenosynovitis. Journal of Bone and Joint Surgery. 2007;89(8):1742-1748.

SAEM Clinical Images Series: A Man with Blurry Vision

cranial nerve

A middle-aged man with a past medical history of hypertension and tobacco use disorder presented to the Emergency Department after evaluation by an ophthalmologist.  He complained of ten days of a right-sided headache and three days of diplopia. He denied eye pain, pain with eye movements, photophobia, and vision loss.

Vitals: Temp 98.4 °F (36.9 °C); BP 122/72; Pulse 90; Resp 16; SpO2 100%

Neuro: Ptosis, “down and out” deviation and pupil dilation of the right eye were noted. Extraocular movements were intact and pupils were reactive to light bilaterally. No other neurologic deficits were observed.

Non-contributory

This patient has a partial cranial nerve (CN) III (oculomotor nerve) palsy. CN III is composed of: (a) internal somatic motor fibers that innervate the levator palpebrae superioris (which elevates the upper eyelid) and the medial recti, superior recti, inferior recti, and inferior oblique extraocular muscles, and (b) external parasympathetic fibers innervating the ciliary muscles (involved in accommodation) and sphincter pupillae (involved in pupillary constriction). The presentation of complete isolated CN III palsy generally involves ipsilateral ptosis (due to levator palpebrae paralysis) and “down and out” ocular deviation (due to preservation of superior oblique and lateral rectus function).

The most common etiology of CN III palsy is ischemia of the nerve fibers secondary to diabetes mellitus or hypertension, which preferentially affects the internal somatic fibers that surround the blood supply. This etiology classically results in a pupil-sparing palsy due to preserved function of the external parasympathetic fibers. However, the most feared etiology is an intracranial aneurysm, most commonly a posterior communicating artery aneurysm. This source of external compression classically affects both the internal somatic motor fibers and external parasympathetic fibers, resulting in asymmetric pupil dilation.

Take-Home Points

  • CN III palsy etiologies include ischemia secondary to diabetes mellitus or hypertension, and structural causes, most commonly a posterior communicating artery aneurysm.
  • On exam, complete CN III palsies will present with ipsilateral ptosis, “down and out” ocular deviation, and pupillary dilation. Partial CN III palsies may have a more subtle presentation.
  • New-onset CN III palsy should be evaluated with a CTA to rule out an aneurysm.

  • Biousse V, Newman NJ. Third nerve palsies. Semin Neurol. 2000;20(1):55-74. doi: 10.1055/s-2000-6833. PMID: 10874777. 2. Singh A, Bahuguna C, Nagpal R, Kumar B. Surgical management of third nerve palsy. Oman J Ophthalmol. 2016 May-Aug;9(2):80-6. doi: 10.4103/0974-620X.184509. PMID: 27433033; PMCID: PMC4932800.

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2021 SAEM Annual Meeting | Copyrighted by SAEM 2021 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2023-08-14T14:10:25-07:00Aug 18, 2023|Neurology, SAEM Clinical Images|

SAEM Clinical Images Series: The Color Purple

purple urine

A 64-year-old female with a history of quadriplegia and bladder rupture secondary to a motor vehicle accident two years ago, complicated by chronic indwelling suprapubic foley, presents from her skilled nursing facility with fever, oliguria, tachycardia, low blood pressure, and a change in the color of her urine.

Vitals: T 100.4°F; HR 126; BP 105/74; RR 24

General: Pleasant but mildly confused morbidly obese female smelling strongly of urine

Genitourinary: Poorly maintained indwelling suprapubic catheter with purulence noted around the ostomy and purple urine in her foley tubing and bag

Urinalysis (UA): 168 WBC, >182 RBC, Large leukocyte esterase, Positive nitrite

This is a case of Purple Urine Bag syndrome (PUBS), an uncommon subset of CAUTI that generally occurs in female patients with constipation and an indwelling foley. Although not fully understood, it is thought that the long stool transit time of constipation allows GI flora to break tryptophan down into indoles which travel to the liver via the portal system where they become indoxyl sulfate, which is excreted into the urine. Bacterial enzymes there catalyze this to indoxyl which oxidizes in alkaline urine to both indigo (blue) and indirubin (red), the combination of which, plus interaction with the plastic catheter tubing, causes the vivid purple discoloration. Risk factors include women, chronically catheterized, elderly, recurrent UTI, institutionalization, and chronic constipation.

Causative organisms are primarily gram-negative and include Proteus mirabilis, Escherichia coli, Klebsiella pneumonia, Pseudomonas aeruginosa, Morganella morganii, and Enterococcus species.

Take-Home Points

  • PUBS is a rare subset of CAUTI primarily caused by gram-negative bacteria.
  • It is predominantly found in women, chronically catheterized, institutionalized, and constipated patients.
  • Treatment is appropriate antibiotics and improved foley hygiene, foley exchange as well as improved bowel regimen to increase stool transit time.
  • Meekins Pauline, Ramsay Amy, Ramsay Michael. Purple Urine Bag Syndrome. West J Emerg Med. 2012 Dec;13(6):499-500. 2. Scleszka Laura, Swan Tricia. October 9, 2020. Can Urine Color Guide Management? [online] EMRA. Available at: https://www.emra.org/emresident/article/purple-urine-bag-syndrome/ [Accessed 19 Dec. 2022]

By |2023-08-14T09:14:36-07:00Aug 14, 2023|Infectious Disease, SAEM Clinical Images|

SAEM Clinical Images Series: Back Yard Football Injury

sternoclavicular

A 10-year-old male with no past medical history presents to the Emergency Department (ED) by EMS for evaluation of an injury sustained while playing tackle football. The patient was forcibly hit by another child against a tree. He complains of sharp right shoulder and chest pain that worsens with movement of his right upper extremity and he arrives wearing a sling to immobilize the arm.

Vitals: BP 123/86; HR 121; RR 25; T 37°C

General: Alert and oriented, in moderate distress

Cardiovascular: RRR without murmurs, rubs, or gallops, peripheral pulses 2+ throughout

Pulmonary:  Bilateral breath sounds, clear to auscultation

Chest: Inability to visualize the right medial clavicular notch or clavicular ridge along with palpable tenderness at the right upper sternoclavicular joint

MSK: The shoulders are asymmetric with the right slightly higher than the left. The right arm is held adducted and internally rotated in a sling. The patient is reluctant to abduct the right arm secondary to pain.

Neuro: No gross motor or sensory deficits were appreciated

Non-contributory

Sternoclavicular (SC) joint dislocation

SC joint dislocation can occur with anterior or posterior displacement of the medial clavicular head. Anterior dislocations are mostly caused by medial impact to the lateral shoulder. Anterior dislocations are more common and generally regarded as less serious. Conversely, posterior dislocations are more serious but less common. Posterior dislocations usually result from impact directly to the anterior chest wall. High-speed motor vehicle accidents or high-impact sports are common causes of posterior dislocations.

Subclavian vascular injury, pneumothorax, esophageal injury, cardiac arrhythmias, brachial plexus injury, tracheal injury, and thoracic outlet syndrome are all potential complications of an SC joint dislocation. When the medial head of the clavicle is forced posteriorly into the superior mediastinum several structures are at risk of impingement which could cause serious complications. In patients with suspicion of clavicular fracture or dislocation, the presence of dyspnea, stridor, dysphagia, or hoarseness should raise genuine concern for a compressive mediastinal syndrome that may require emergent closed or surgical relocation attempts.

Take-Home Points

  • An anterior medial head sternoclavicular dislocation is generally apparent and easily palpable on physical examination, while a posterior dislocation may be difficult to appreciate.
  • A posterior medial head sternoclavicular dislocation may require computed tomography to diagnose and requires computed tomography angiography to fully assess all mediastinal structures.
  • Closed reduction is the gold standard for the treatment of non-complicated posterior dislocations. Surgical fixation may be required when compressive complications such as vascular injury are confirmed or when closed reduction is unsuccessful.
  • Patients with a previous history of sternoclavicular dislocation are at higher risk of developing thoracic outlet syndrome.

SAEM Clinical Images Series: My Eye Looks Different

cone

A 29 year-old-male with a past medical history of left eye enucleation secondary to a gunshot wound several years prior presents to the Emergency Department (ED) for blurry vision, redness, and concern for a deformity to his right eye. The patient states symptoms started 2-3 months ago and he initially thought symptoms were due to allergies and recalls rubbing his eye a lot. Over the past 3-4 days, he noticed an acute decline in his vision with what the patient describes as a “cloudy bump” appearing during that time. The patient normally does not wear contacts or corrective lenses but states his vision is very blurry and he is now having difficulty reading. He also reports photophobia and mild eye pain. Review of systems is negative for any fevers, headache, eye discharge, or any recent falls or trauma.

Vitals: BP 125/83; Pulse 70; Temp 97.6 F (36.4 C); Resp 17; SpO2 100%

Constitutional: No acute distress, lying in stretcher comfortably.

Head: No visible traumatic injuries. No peri-orbital edema or facial swelling.

Eyes:

  • OD: Edematous cone-shaped protrusion with central haziness. V-shaped deformity to lower lid margin noted on downward gaze. The patient reports no pain when performing extraocular movement testing which is intact and pupil is reactive to light. Visual fields intact. There is no fluorescein uptake upon Wood’s Lamp exam and IOP is 18. VisualAcuity OD 20/200.
  • OS: Eye prosthesis in place.

Nose: No foreign bodies.

Mouth/Throat: Oropharynx is clear and moist and mucous membranes are normal.

Neck: Normal range of motion.

Corneal hydrops secondary to keratoconus.

Keratoconus is a degenerative, multifactorial, non-inflammatory disorder of the cornea that causes bilateral thinning of the cornea and distorted vision. The corneal thinning leads to a structural weakness in the collagen fibers that causes the characteristic bulging, “cone-shaped” cornea. If the thinning is significant enough, a break in collagen fibers and Descemet’s membrane lead to sudden edema which appears as a corneal opacification. This complication is known as corneal hydrops and causes sudden eye pain and decreased visual acuity. Patients with keratoconus present in young adulthood with progressive blurry or distorted vision. Risk factors include connective tissue disorders and Down syndrome as well as a familial history of keratoconus. There is also a risk in patients with a history of eye rubbing as was the case with this patient. The initial treatment for keratoconus is corrective eyewear for refractive correction.

The clinical hallmark of keratoconus is the cone-like protrusion of the cornea. The bulging may eventually lead to “Munson’s sign”, a v-shaped indentation of the lower eyelid on downward gaze as the cornea bulges outward that is seen in advanced keratoconus.

Take-Home Points

  • Suspect keratoconus in patients with a history of constant eye rubbing, developmental delay (i.e. Down Syndrome), and in patients with connective tissue disorders.
  • Munson’s Sign is a v-shaped indentation of the lower eyelid on downward gaze as the cornea bulges outward.
  • Initial treatment of keratoconus is conservative management with prompt ophthalmology follow-up.

  • V. Mas Tur, C. MacGregor, R. Jayaswal, D. O’Brart, N. MaycockA review of keratoconus: Diagnosis, pathophysiology, and genetics Surv Ophthalmol, 62 (6) (2017), pp. 770-783
  • Gold J, Chauhan V, Rojanasthien S, Fitzgerald J. Munson’s Sign: An Obvious Finding to Explain Acute Vision Loss. Clin Pract Cases Emerg Med. 2019 Jul 8;3(3):312-313. doi: 10.5811/cpcem.2019.5.42793. PMID: 31403106; PMCID: PMC6682229.
  • Gialousakis, John P. “Management of Acute Corneal Hydrops in a Patient with Keratoconus: a Teaching Case Report.” The Journal of the Association of Schools and Colleges of Optometry, vol. 45, 2020.
  • Greenwald MF, Vislisel JM, Goins KM. Acute Corneal Hydrops. EyeRounds.org. August 3, 2016; Available from: http://EyeRounds.org/cases/241-acute-corneal-hydrops.htm
  • Stack L, Sheedy C, Bales B. Corneeal Hydrops: A Complication of Keratoconus. Visual Diagnosis Ophthalmology. Published 2015 Dec 11. Available from: https://www.emra.org/emresident/article/corneal-hydrops-a-complication-of-keratoconus/

By |2023-04-05T14:07:32-07:00Apr 17, 2023|HEENT, Ophthalmology, SAEM Clinical Images|

SAEM Clinical Images Series: A Rare Pediatric Scalp Rash

rash

The patient is a 3-month-old, full-term male who presents with a rash on his head. The rash started one day prior to presentation on his forehead and spread to the rest of his head. Today, it developed a central clearing with surrounding redness. He has a history of sensitive skin since birth with patches of eczema and cradle cap. He treats these with Aquaphor and Honest Co. Cream; he has never been prescribed topical steroids for his rashes. Denies fever, cough, rhinorrhea, congestion, decreased appetite, diarrhea, and decreased urination. He had an uncomplicated birth history.

General: Well appearing, no distress.

Skin: Large, serpiginous rash on the left forehead and scalp with central clearing and peripheral erythema as well as areas of erythematous plaques. He has some erythema of the left medial epicanthus. He also has a large erythematous patch at the base of his skull. The remainder of his skin is clear.

CV: Normal rate and rhythm, no murmur.

White blood cell (WBC) count: 8.4

Hemoglobin: 12.4

Hematocrit: 37.1

Platelet Count: 468

Complete metabolic panel (CMP): ALT 30, AST 60, Alk phos 266, Tbili 0.7, Total Protein 6.4

The image is of the cutaneous manifestation of neonatal lupus erythematosus. Neonatal lupus erythematosus is an autoimmune disease caused by transplacental passage of maternal autoantibodies to Sjögren’s syndrome A or B autoantigens (SS-A/SS-B). It can present with reversible changes including cutaneous lesions (most common, in up to 40% of patients), hepatobiliary disease, and cytopenias, which resolve once maternal autoantibodies have been cleared.

All infants that present with concern for neonatal lupus erythematosus should have screening labs performed to evaluate for hematologic, cardiac, and hepatobiliary involvement including a CBC with differential, liver enzymes, and antibody testing. In addition, an EKG is essential given that neonates can present with irreversible total atrioventricular heart block, which can present in utero or after birth.

The rash typically presents in the first few weeks of life but can present as late as 2-3 months of life (usually within 1-2 days of first sun exposure). Eighty percent of cases are not clear at birth and present in the first month of life. The rash appears as a coalescing rash with raised margins, with annular and discoid erythema involving the head in 95% of cases. It is often misdiagnosed as skin infections or eczema if the mom is asymptomatic. Fifty percent resolve by four months of life and 100% by one year.

Any neonate with a slow fetal heart rate or the postnatal diagnosis of atrioventricular heart block warrants immediate maternal testing for these autoantibodies. Most cardiac changes from neonatal lupus are diagnosed before 26 weeks gestation, with <20% later in pregnancy and 2% detected postnatally.

Take-Home Points

  • While cutaneous findings of neonatal lupus most commonly present in the first month of life, they can present as late as 2-3 months.
  • The cutaneous findings associated with neonatal lupus most of the time resolve in 4-6 months (when maternal antibodies are cleared from the infant’s circulation).
  • Any baby with findings concerning for neonatal lupus should have an EKG performed. Around 2% of infants present with heart block postnatally within the first month.

  • Diaz-Frias J, Badri T. Neonatal Lupus Erythematosus. [Updated 2021 Jun 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK526061/
  • Lee LA. Neonatal lupus erythematosus: clinical findings and pathogenesis. J Investig Dermatol Symp Proc. 2004 Jan;9(1):52-6. doi: 10.1111/j.1087-0024.2004.00827.x. PMID: 14870986.

By |2023-04-05T14:00:29-07:00Apr 10, 2023|Dermatology, Pediatrics, SAEM Clinical Images|
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