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About Andrew Mittelman, MD

Assistant Professor of Emergency Medicine
Boston Medical Center

SAEM Clinical Images Series: A Grain of Sand… or Something More Sinister?

hsv

A 54-year-old male with a history of Type 2 Diabetes Mellitus presented with one day of atraumatic left eye pain. He reports pain with blinking and a sandy foreign body sensation. Patient denies new discharge from the eye, though endorses increased tearing. He reports no recent trauma to the face or chemical exposures. He has had no recent rashes or sick contacts and no associated infectious symptoms. Patient does not wear contact lenses.

Vitals: BP 159/98, HR 73, Temp 98.2°F (36.8°C), RR 16, SpO2 97%

HEENT: PERRL. EOMI. Left conjunctiva injected. Right conjunctiva normal. No discharge. No rashes or lesions. Ocular exam following fluorescein administration shown in image.

Glucose: 90 mg/dL

HSV Keratitis

Administration of fluorescein reveals punctate or diffuse branching ulceration (herpetic dendrites) on the cornea, as shown in this case.

This patient has herpes simplex virus (HSV) keratitis. Primary ocular HSV infection is usually caused by direct contact with contaminated secretions or lesions and most frequently presents as epithelial disease. Epithelial keratitis can manifest clinically as unilateral eye pain, redness, tearing, and foreign body sensation. Once affected, patients are at risk for chronic reactivation, which may be triggered by fever, trauma, menstruation, stress, or trigeminal nerve manipulation. Importantly, infectious and immunocompromised conditions predispose to reactivation. Therefore, it is essential to screen for underlying stressors such as hyperglycemia and HIV. Administration of fluorescein reveals punctate or diffuse branching ulceration (herpetic dendrites) on the cornea, as shown in this case.

The diagnosis of HSV is often made clinically, though laboratory testing of conjunctival scrapings, cytology specimens, and vesicular skin lesions may be conducted. If readily available, ophthalmology should be consulted to determine the depth of corneal involvement and associated sequelae of HSV. First line treatment for HSV keratitis includes oral antiviral treatment with acyclovir, valacyclovir, or famciclovir for 10-14 days and/or topical antiviral medications including topical ganciclovir 0.15% or trifluridine 1%. Long- term prophylaxis with oral antivirals is often considered, notably for patients at high risk of recurrence. Without adequate treatment, HSV keratitis can lead to severe vision impairment and is the leading cause of corneal blindness worldwide. All patients need urgent/emergent ophthalmology follow-up within 24 hours.

Take-Home Points

  • Primary ocular HSV-1 keratitis is a leading preventable cause of blindness and classically presents with unilateral eye pain, foreign body sensation, and corneal herpetic dendrites on fluorescein exam.
  • Avoid using topical steroids as monotherapy because they can suppress the patient’s immune response, allowing the herpes virus to replicate more readily, which may cause severe corneal damage, inflammation, and tissue necrosis within the stroma of the cornea. Adjuvant steroids with antiviral therapy have shown to be effective.
  • It is essential to screen for infections and underlying conditions such as HIV as immunocompromised individuals are predisposed to HSV reactivation.

  • Labib BA, Chigbu DI. Clinical Management of Herpes Simplex Virus Keratitis. Diagnostics (Basel). 2022 Sep 29;12(10):2368. doi: 10.3390/diagnostics12102368. PMID: 36292060; PMCID: PMC9600940.
  • Arshad S, Petsoglou C, Lee T, Al-Tamimi A, Carnt NA. 20 years since the Herpetic Eye Disease Study: Lessons, developments and applications to clinical practice. Clin Exp Optom. 2021;104(3):396-405.
  • Sugar, A. 2024, Apr 10. Herpes simplex keratitis. UpToDate. Retrieved January 2, 2024, from https://www.uptodate.com/contents/herpes-simplex-keratitis?search=hsv%20keratitis&source=search_result&selectedTitle=1%7E150&usage_type=default&display_rank=1#H3848962064

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Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2025 SAEM Annual Meeting | Copyrighted by SAEM 2025 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2026-02-19T12:56:37-08:00Feb 27, 2026|Uncategorized|
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SAEM Clinical Images Series: A Pedunculated Bone to Pick

knee

The patient is a 46-year-old male with a past medical history of chronic left knee pain, hypertension, and congestive heart failure who presents to the Emergency Department with worsening left knee pain. He had been walking more frequently of late to increase his exercise, but denies any falls or specific trauma. He noticed some swelling to the area over the past few days but there has been no redness, rash, or fever. He also denies calf pain, lower leg swelling, and shortness of breath. He has no other complaints at this time but due to his worsening
pain and mild swelling, he comes in for evaluation.

 

Vital Signs: All vital signs are normal.
General: Well appearing, no acute distress.
Cardiovascular: No murmurs, 2+ peripheral pulses in all extremities.
Extremities: Left knee exam shows a small suprapatellar effusion and mild tenderness to palpation; there is no erythema, deformity, or crepitus; he has full active and passive range of motion.

The patient has an osteochondroma.

Asymptomatic growths require no intervention. Symptomatic patients should be referred to orthopedics for consideration of resection.

Osteochondromas are the most common benign bony tumor and occur due to hamartomatous growth of cartilage. The characteristic x-ray appearance is a sessile or pedunculated bony growth located in the metaphysis projecting away from the epiphysis, as seen in this case. These lesions are more commonly seen in males and are typically diagnosed in the first four decades of life, with 75% of diagnoses occurring before the age of twenty. Patients typically present with painless masses close to tendon insertion sites, most commonly near the knee. There is a low risk of malignant transformation. Patients with Multiple Hereditary Exostoses, a rare autosomal dominant genetic condition, may present with numerous osteochondromas with a greater potential for malignant transformation. While the majority of osteochondromas are asymptomatic, symptoms may develop due to impingement on nearby structures or from fractures. If patients have persistent symptoms or cosmetic concerns, they can be referred to orthopedic surgery for consideration of resection. There have been no approved medical therapy options for osteochondroma.

Take-Home Points

  • Osteochondromas are benign bony tumors that typically present as painless masses and are also commonly found incidentally on x-ray.
  • Treatment is usually supportive; however, orthopedic surgery referral should be considered for persistent or severe symptoms.

  • Paras T, O’Donnell P. Osteochondroma & Multiple Hereditary Exostosis. Orthobullets.   Rauf A, Gaillard F. Osteochondroma. In: Radiopaedia.Org. Radiopaedia.org; 2005. doi:10.53347/rID-1799
  • Tepelenis K, Papathanakos G, Kitsouli A, et al.   Osteochondromas: an updated review of epidemiology, pathogenesis, clinical presentation, radiological features and treatment options. In Vivo. 2021;35(2):681-691. doi:10.21873/invivo.12308

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Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2025 SAEM Annual Meeting | Copyrighted by SAEM 2025 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2026-01-06T10:24:09-08:00Jan 12, 2026|SAEM Clinical Images|
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SAEM Clinical Images Series: Tangled in the Toilet

An otherwise healthy 46-year-old male presented to the Emergency Department with 18 months of diarrhea and intermittent abdominal cramping that has acutely worsened in the past week. On the morning of presentation, he noticed a worm-like object in his stool, which he brought to the ED (See images), prompting his visit. Throughout these 18 months, he experienced 4-10 loose bowel movements per day. He tried dietary modifications, including the removal of dairy, gluten, and soy, all without relief. The patient frequently travels for work, mainly to the US, Europe, and intermittently to Asia. His diet includes all forms of meat, fish, and shellfish. He denied fevers, chills, headaches, chest pain, shortness of breath, unexpected weight loss or gain, nausea, vomiting, or changes in his urinary habits. His stool has been non- greasy and has not contained any blood or mucous.

Vitals: BP 136/85; HR 70; R 18; T 98.2°F; O2 sat; 97% room air.

General: Well appearing, no acute distress.

Abdomen: There is mild tenderness to palpation in bilateral lower quadrants. Bowel sounds present in all quadrants. No rebound tenderness or guarding. No organomegaly.

Lymph: No lymphadenopathy present.

Skin: No rashes.

WBC: 5.4

Hgb: 14.4

Dibothriocephalus (Diphyllobothrium) latus: a tapeworm.

Stool ova and parasites.

This patient is infected with Dibothriocephalus (Diphyllobothrium) latus, a tapeworm distinctive for its proglottids with central hyperpigmented reproductive organs, as shown in the images. Patients rarely visualize the tapeworm in their stool, so diagnosis is usually made with a stool ova and parasite study. Diphyllobothrium latus infection is commonly caused by eating raw, undercooked, or lightly pickled seafood contaminated with tapeworm eggs. Tapeworm eggs are also occasionally used as weight loss supplements. The market for these supplements is not regulated; thus, the eggs may be from other parasites, leading to more severe manifestations of infection in different body areas, such as the brain, lungs, or muscles. Diphyllobothrium latus infection can cause pernicious anemia, as 80% of Vitamin B12 intake may be absorbed by the worm. Treatment for Diphyllobothrium latus is a single dose of praziquantel. Due to fecal-oral transmission, patients who engage in high risk transmission-prone behaviors should consider having their partners tested and treated as well.

Take-Home Points

  • Diphyllobothrium latus infection may cause Vitamin B12 deficiency and resultant anemia as the worm may absorb up to 80% of B12 intake.

  •  A single dose of praziquantel is generally sufficient to eradicate tapeworm infection.

  • Schantz, P. M. (1996). Tapeworms (cestodiasis). Gastroenterology Clinics of North America., 25(3), 637–653. https://doi.org/10.1016/s0889-8553(05)70267-3
  • Craig P, Ito A. Intestinal cestodes. Curr Opin Infect Dis. 2007 Oct;20(5):524-32. doi: 10.1097/QCO.0b013e3282ef579e. PMID: 17762788
  • Scholz T, Garcia HH, Kuchta R, Wicht B. Update on the human broad tapeworm (genus Diphyllobothrium), including clinical relevance. Clin Microbiol Rev. 2009; 22:146–160

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2025 SAEM Annual Meeting | Copyrighted by SAEM 2025 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2025-10-26T13:38:34-07:00Oct 31, 2025|Infectious Disease, SAEM Clinical Images|
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SAEM Clinical Images Series: First a Splash and then a Rash

rash

The patient is a 25-year-old female with no significant past medical history who presents to the Emergency Department with a pruritic rash. She reported three days of progressive pruritus with an associated diffuse rash extending from the lower extremities to the proximal upper extremities with involvement of the chest and back. She denies fevers, chills, difficulty breathing, nausea, vomiting, or history of similar rash. She has no history of dermatologic or immunologic conditions. She has had no new exposures to new soaps or chemicals. She has no known allergies, is up to date on all vaccinations, and has not traveled in the last year other than a day trip to an indoor water park three days ago.

None

Vitals: Normal

General: No acute distress but uncomfortable from itching.
HEENT: Oropharynx clear without edema, erythema, or mucosal lesions.
Respiratory: Clear to auscultation bilaterally.
Skin: Key findings as shown in the image provided. There is a diffuse papular rash extending from the bilateral distal lower extremities up to level of the sternum with uniform involvement of the abdomen, chest, back, and upper extremities. Negative Nikolsky’s sign. No involvement of the head, neck, palms of the hands, or soles of the feet.

Pseudomonas aeruginosa folliculitis (“Hot Tub folliculitis”)

Pseudomonas aeruginosa, fluoroquinolones

This patient presented with a history and exam classic for Pseudomonas aeruginosa folliculitis, or “hot tub” folliculitis. The primary risk factor for this condition is exposure to contaminated water, typically via public swimming pools or hot tubs with inadequate chlorine levels. Longer durations of exposure, female gender, and underlying skin trauma are additional risk factors. The infection is associated with a tender and pruritic rash which begins as papules and can progress to papulopustular or nodular lesions. The rash may develop on any body part that is exposed to the contaminated water. Symptoms classically begin within 8 to 48 hours of the initial exposure, however can develop up to five days later. A subset of patients may develop systemic symptoms of malaise and fever. Most cases are self-limited, resolving without treatment in one to two weeks. However, patients with significant cutaneous involvement or discomfort, systemic symptoms, or immunocompromised state should be treated empirically with an oral fluoroquinolone. Symptomatic

Take-Home Points

  • In patients presenting with follicular rashes, be sure to ask about public pool or hot tube exposures.
  • Hot tub folliculitis is a pseudomonas infection and can be treated with oral fluroquinolones.

1. Centers for Disease Control and Prevention (CDC). Pseudomonas dermatitis/folliculitis associated with pools and hot tubs–Colorado and Maine, 1999-2000. MMWR Morb Mortal Wkly Rep. 2000;49(48):1087-1091.

2. Tate D, Mawer S, Newton A. Outbreak of Pseudomonas aeruginosa folliculitis associated with a swimming pool inflatable. Epidemiol Infect. 2003;130(2):187-192. doi:10.1017/s0950268802008245

3. Jacob JS, Tschen J. Hot Tub-Associated Pseudomonas Folliculitis: A Case Report and Review of Host Risk Factors. Cureus. 2020;12(9):e10623. Published 2020 Sep 23. doi:10.7759/cureus.10623

4. Silverman AR, Nieland ML. Hot tub dermatitis: a familial outbreak of Pseudomonas folliculitis. J Am Acad Dermatol. 1983;8(2):153-156. doi:10.1016/s0190-9622(83)70017-4

5. Luelmo-Aguilar J, Santandreu MS. Folliculitis: recognition and management. Am J Clin Dermatol. 2004;5(5):301-310. doi:10.2165/00128071-200405050-00003

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2025 SAEM Annual Meeting | Copyrighted by SAEM 2025 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2025-10-27T08:34:29-07:00Oct 24, 2025|Dermatology, SAEM Clinical Images|
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SAEM Clinical Images Series: Weird Flex

tenosynovitis

A 29-year-old female with a history of depression, anxiety, and tobacco use disorder presented with worsening right index finger pain, swelling, and redness for the previous three days. Additionally, she reported that she was unable to further flex or extend her finger. She denied fevers, chills, rashes, or recent illness. There was no history of trauma, aquatic or other environmental exposures, insect bites, or intravenous drug use. She did note that she uses a copper brillo pad to clean her dishes at home which often causes small abrasions to her fingers.

Vitals: BP 160/112; PR 73; Temp 36.4°C; RR 18; SpO2 100% on RA

General: Well-appearing, no acute distress.

Cardiovascular: Right index finger capillary refill <2 sec.

Skin: Right index finger uniformly edematous and erythematous with tenderness to palpation along the tendon sheath; small healed abrasions over distal palmar aspect of the digit; no focal area of fluctuance.

MSK: right index finger held in flexion, pain with passive extension.

WBC: 8.6

ESR: 129

CRP: 105.5

This patient has flexor tenosynovitis, an infection of the synovial sheath surrounding the flexor tendon of the hand. The condition is usually caused by local inoculation from penetrating trauma although can also result from hematogenous spread. Flexor tenosynovitis is considered a surgical emergency, as delayed intervention can lead to significant morbidity including tendon rupture, deep space infection, abscess development, soft tissue necrosis, amputation, and/or chronically compromised hand function. Diagnosis is usually clinical, based on history and physical exam findings; however, laboratory evaluation may reveal leukocytosis and/or elevated inflammatory markers. If there is a history of penetrating trauma, x-rays of the affected digit are recommended to rule out retained foreign body. Management in the ED includes prompt surgical consultation and broad-spectrum antibiotics against common cutaneous pathogens. Antibiotic coverage should be broadened in patients with a history of marine exposure or Pseudomonal risk factors including immunocompromised status.

Flexor tenosynovitis presents with four classic exam findings called “Kanavel Signs.” Kanavel Signs include (1) flexion of the involved digit, (2) tenderness to palpation over the tendon sheath, (3) pain with passive extension, and (4) uniform swelling of the finger. The presence of all four Signs has a sensitivity for flexor tenosynovitis as high as 97.1%, although early in the course of infection, pain with passive extension may be the only finding.

Take-Home Points

  • Flexor tenosynovitis is an infection of the flexor tendon sheath of the hand and a history of trauma or penetrating injury to the area should raise suspicion.

  • Flexor tenosynovitis is a “can’t miss” clinical diagnosis in the ED as there is a risk of significant complications with delayed antibiotics and surgical intervention.

  • Infection can reliably be identified by the presence of the four Kanavel Signs on physical exam.

  • Chan E, Robertson BF, Johnson SM. Kanavel signs of flexor sheath infection: a cautionary tale. Br J Gen Pract. 2019 Jun;69(683):315-316. doi: 10.3399/bjgp19X704081. PMID: 31147342; PMCID: PMC6532803.

  • Chapman T, Ilyas AM. Pyogenic Flexor Tenosynovitis: Evaluation and Treatment Strategies. J Hand Microsurg. 2019 Dec;11(3):121-126. doi: 10.1055/s-0039-1700370. Epub 2019 Nov 2. PMID: 31814662; PMCID: PMC6894957.

  • Hermena S, Tiwari V. Pyogenic Flexor Tenosynovitis. In: StatPearls. StatPearls Publishing; 2022.

  • Kennedy CD, Huang JI, Hanel DP. In Brief: Kanavel’s Signs and Pyogenic Flexor Tenosynovitis. Clin Orthop Relat Res. 2016 Jan;474(1):280-4. doi: 10.1007/s11999-015-4367-x. Epub 2015 May 29. PMID: 26022113; PMCID: PMC4686527.

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2023 SAEM Annual Meeting | Copyrighted by SAEM 2023 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2025-03-30T20:30:57-07:00Apr 7, 2025|Orthopedic, SAEM Clinical Images|
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SAEM Clinical Images Series: Ptosis? A Don’t Miss Diagnosis!

ptosis

A 50-year-old female with no past medical history presented to the emergency department for a headache. She developed progressive dull, left-sided head pain with sinus pressure one week prior, associated with sleep disturbance. In addition, she described two days of left eyelid drooping. She had no fever, chills, cough, difficulty breathing, neck pain, jaw claudication, vision changes, dizziness, numbness, or recent weight loss. She also denied any recent trauma to the head or neck.

 

Vitals: BP 119/59; PR 92; Temp 37°C; RR 16; SpO2 100% on RA

General: Well-appearing, no acute distress.

HEENT: EOMI, left eyelid ptosis with miosis of left pupil.

Cardiovascular: RRR, normal S1/S2, no murmur.

Neurologic: Alert and oriented x 3, normal strength and sensation bilateral upper and lower extremities, left ptosis and miosis, otherwise cranial nerves II-XII unremarkable.

WBC: 8.9

INR: 0.9

This patient presented with Horner Syndrome, a triad of ipsilateral anhidrosis, miosis, and ptosis, the latter two of which are evident in this clinical image. Horner Syndrome presents when a lesion or insult disturbs the three-order sympathetic pathway that innervates the head, neck, and ipsilateral eye. Physical examination findings may be variable and/or subtle in patients with carotid dissection. Interestingly, isolated Horner Syndrome is the only abnormal physical finding in up to 50% of patients with carotid dissection. Further, patients with carotid dissection may present with only a partial Horner’s, with anhidrosis limited to the ipsilateral eyebrow, which can be difficult to identify. Evaluation of a patient with a new Horner Syndrome in the emergency department should include CT brain, CXR, and, if there is concern for carotid artery dissection, CTA or MRA head/neck. Carotid artery dissection is a neurologic emergency with significant morbidity and mortality ranging between 25-46% if left untreated. Management requires emergent neurology consultation with activation of the stroke team, as the treatment may require systemic thrombolytics and/or mechanical thrombectomy. Patients who present outside the time-window for stroke care, or who demonstrate resolving symptoms should be treated with antiplatelet or anticoagulant therapy. Notably, for patients with intracranial dissection or dissection involving the aorta, the preferred treatment is antiplatelet therapy in conjunction with neurology consultation.

Horner syndrome has a broad differential diagnosis including stroke, neoplastic disease (brain, neck or lung), vascular injury, demyelinating disease, lymphoma, and iatrogenic injuries. This patient’s Horner syndrome was attributable to a carotid artery dissection (the most common vascular cause of Horner’s). Carotid dissection may occur after blunt trauma to the neck, but also as a result of seemingly innocuous movements of the neck. For example, evidence suggests that yoga, massage, and roller coaster rides each may increase risk for carotid dissection.

Take-Home Points

  • Horner syndrome is the triad of ipsilateral anhidrosis, miosis, and ptosis, although physical exam findings may be subtle.

  • The differential for Horner Syndrome includes several urgent and emergent underlying etiologies.

  • Carotid artery dissection is an important cause of Horner Syndrome to consider in the appropriate clinical context.

  • Hakimi R, Sivakumar S. Imaging of Carotid Dissection. Curr Pain Headache Rep. 2019 Jan 19;23(1):2. doi: 10.1007/s11916-019-0741-9. PMID: 30661121.

  • Keser Z, Chiang CC, Benson JC, Pezzini A, Lanzino G. Cervical Artery Dissections: Etiopathogenesis and Management. Vasc Health Risk Manag. 2022 Sep 2;18:685-700. doi: 10.2147/VHRM.S362844. PMID: 36082197; PMCID: PMC9447449.

  • Flaherty PM, Flynn JM. Horner syndrome due to carotid dissection. J Emerg Med. 2011 Jul;41(1):43-6. doi: 10.1016/j.jemermed.2008.01.017. Epub 2008 Sep 14. PMID: 18790590.

  • Maloney WF, Younge BR, Moyer NJ. Evaluation of the causes and accuracy of pharmacologic localization in Horner’s syndrome. Am J Ophthalmol. 1980 Sep;90(3):394-402. doi: 10.1016/s0002-9394(14)74924-4. PMID: 7425056.

  • Stein DM, Boswell S, Sliker CW, Lui FY, Scalea TM. Blunt cerebrovascular injuries: does treatment always matter? J Trauma. 2009 Jan;66(1):132-43; discussion 143-4. doi: 10.1097/ TA.0b013e318142d146. PMID: 19131816.

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Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2023 SAEM Annual Meeting | Copyrighted by SAEM 2023 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2025-04-03T09:22:20-07:00Apr 4, 2025|Neurology, SAEM Clinical Images|
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SAEM Clinical Images Series: An Unusual Arm Conundrum

shoulder

A 58-year-old female with a past medical history significant for osteoporosis presented with right shoulder pain after a witnessed mechanical fall down two stairs. She sustained no headstrike or loss of consciousness. She endorses severe right shoulder pain without numbness/tingling over any part of her arm. Since the fall, she has been unable to move her arm, which remains abducted overhead.

 

dislocation

General: Right arm fixed, abducted position and elevated over her head.

Vascular: 2-second capillary refill in all nail beds, strong palpable radial pulse.

Neuro: Sensation intact to light touch on medial and lateral aspects of all distal digits, and throughout entire axillary, radial, ulnar and median nerve distribution.

Motor: Flexor digitorum superficialis (FDS) and flexor digitorum profundus (FDP) intact in digits 2 through 5. Extensor digitorum communis (EDC) and extensor indicis proprius (EIP) intact. Normal finger abduction and adduction. Normal thumb opposition. Normal OK sign. Wrist flexors and extensors intact.

None

Luxatio erecta (inferior shoulder dislocation) is a rare type of shoulder dislocation. The majority of shoulder dislocations are anterior (over 95%), with a smaller number being posterior (2-4%). Inferior dislocations are the least common injury pattern (0.5%), but prompt identification and treatment are crucial due to the high risk of neurovascular damage.  Radiographs will typically demonstrate the humeral head lying inferior to the glenoid fossa, with the humeral shaft parallel to the spine of the scapula. Classically, the entire arm is held in abduction.

Inferior shoulder dislocation most commonly occurs either due to hyperabduction of the shoulder (such as when grasping at a tree branch above while falling) or through an axial load from above on a hyperabducted arm (as seen in falls or motor vehicle accidents). Patients presenting with inferior shoulder dislocation are at substantial risk for neurovascular compromise, particularly of the axillary nerve, leading to impaired upper extremity movement and sensation. Due to the substantial injury mechanism, patients with inferior shoulder dislocations are also at increased risk for rotator cuff pathology. Treatment of inferior shoulder dislocation is immediate closed reduction to reduce the risk of neurovascular complications. Once reduced, the arm should be placed in an immobilizer to prevent recurrent dislocation.

Take-Home Points

  • Patients with inferior shoulder dislocations often present holding their arm above their head. Often, patients cannot adduct their arm.

  • Axillary nerve injuries occur in about 60% of inferior dislocations. Compared to other dislocations, inferior dislocations have the highest incidence of axillary nerve injuries.

  • Patients with inferior dislocations often present with neurovascular compromise of the affected arm, so be sure to do a thorough exam after reduction.

  • Grate I Jr. Luxatio erecta: a rarely seen, but often missed shoulder dislocation. Am J Emerg Med. 2000 May;18(3):317-21. doi: 10.1016/s0735-6757(00)90127-x. PMID: 10830689.

  • Nambiar M, Owen D, Moore P, Carr A, Thomas M. Traumatic inferior shoulder dislocation: a review of management and outcome. Eur J Trauma Emerg Surg. 2018 Feb;44(1):45-51. doi: 10.1007/s00068-017-0854-y. Epub 2017 Oct 3. Erratum in: Eur J Trauma Emerg Surg. 2018 Feb;44(1):53. doi: 10.1007/s00068-017-0878-3. PMID: 28975397.

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2023 SAEM Annual Meeting | Copyrighted by SAEM 2023 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2025-03-09T21:48:15-07:00Mar 10, 2025|Orthopedic, SAEM Clinical Images|
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