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SAEM Clinical Images Series: Spontaneous Eye Luxation

eye

A 55-year-old female presented with the complaint of “my right eye popped out.” Symptoms started approximately seven hours prior to arrival and progressive, severe pain eventually prompted her visit to the ED. This happened once 10 years ago, requiring reduction in the ED. The patient denied preceding trauma, rubbing her eyes/eye-lids, or any history of thyroid disease. She endorsed right eye blurred vision and severe pain.

 

Vitals: HR 86; RR 16; SpO2 97% on room air; BP 179/111

General: Appears uncomfortable

Head: Atraumatic

Ocular:

OD: globe luxation with severe injection and chemosis. Severe corneal dryness. Pupil appears 3mm, minimally reactive, though poor view of pupil secondary to exposure keratopathy. Upper and lower lids inverted beneath globe. IOP 21. Unable to assess extraocular movements

OS: appears grossly normal. Pupil 3mm and reactive. Full extraocular movements.

Thyroid stimulating hormone and thyroxine within normal limits.

Spontaneous globe luxation (SGL). Luxation of the globe is characterized by the anterior displacement of the globe beyond the orbital rim [1], as seen in photo one. Though SGL is a rare condition, risk factors include proptosis, shallow orbits, or space-invading retrobulbar lesions [2]. Case study reports have also indicated trauma and frequent eyelid manipulation as causes of globe luxation [1].

After assuring adequate anxiolysis and analgesia with IV medications and tetracaine eye drops, the patient should be placed in a supine position. To reduce the globe, the eyelids should be extracted from behind the globe and retracted outwards while direct and even pressure is applied to the globe with damp gauze. For our patient, a lateral tarsorrhaphy was performed by ophthalmology at the bedside given severe keratopahy, lagopthalmos (as seen in photo two), and re-subluxation with Valsalva. Given the unknown etiology of the luxation, thyroid laboratory testing and orbit computed tomography were performed, which were unremarkable. The patient was discharged from the emergency department with tobradex ointment and ophthalmology follow-up in one week

Take-Home Points

  • Immediate reduction of a luxed globe is paramount.

  • Consider topical anesthetic drops and IV analgesia and/or anxiolytics to help assist with patient discomfort and dry eye.

  • Consider labs and imaging to assess for any underlying etiology of spontaneous globe luxation.

  • Kelly, E.W. and Fitch, M.T. (2013) Recurrent Spontaneous Globe Subluxation: A Case Report and Review of Manual Reduction Techniques. Available at: https://www.sciencedirect.com/science/article/abs/pii/S0736467911011462 (Accessed: 04 January 2024).

  • Yadete, T. et al. (2021) Spontaneous globe subluxation: A case report and review of the literature – international journal of emergency medicine, BioMed Central. Available at: https://intjem.biomedcentral.com/articles/10.1186/s12245-021-00398-x (Accessed: 04 January 2024).

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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 |2025-01-06T21:18:46-08:00Jan 13, 2025|Ophthalmology, SAEM Clinical Images|
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SAEM Clinical Images Series: A Curious Case of Anisocoria

anisicoria

A 3-month-old male with no past medical history was brought to the emergency department for evaluation of newly asymmetric pupils. The infant appeared to be asymptomatic per parents, without any behavior changes or associated symptoms noted. The patient’s mother noticed her son’s left pupil was dilated and unresponsive to light the morning of presentation. The father had applied a prescription antiperspirant containing glycopyrronium to his axillae the previous evening but denied any known exposure to the infant.

Vitals: BP 85/66; HR 143; RR 42; SpO2 100%; T 98.3°F

Constitutional: No distress, well appearing.

HENT: Left pupil fixed and dilated to 7 mm in the light and the dark; right pupil 2 mm and reactive in the light, 5 mm in the dark. EOM intact bilaterally. No stigmata of trauma. Normal TMs bilaterally.

Neck: Normal range of motion.

Cardiovascular: Normal rate, regular rhythm and normal heart sounds.

Pulmonary: Breath sounds normal, no respiratory distress.

Abdominal: Soft, nontender, nondistended.

Neurological: Alert. Moving all 4 extremities spontaneously. Normal muscle tone. Normal suck and Moro reflexes.

Skin: Normal. No piloerection or sweating. No bruising or lesions.

No labs drawn. Head CT was obtained, which showed no acute intracranial pathology.

Ophthalmology consultation was sought, and an ophthalmologic exam demonstrated unremarkable slit lamp and fundal exams, with no afferent pupillary defect by reverse. The patient’s anisocoria was ultimately attributed to inadvertent glycopyrronium exposure from his father’s prescription antiperspirant, Qbrexza. The patient’s father later noted that he cradled the patient against his chest after applying the antiperspirant, and was not wearing a shirt at the time

Pilocarpine, a cholinergic antagonist that stimulates pupillary constriction, can be used to test mydriatic pupils. Pilocarpine drops will not reverse pharmacologically-induced anisocoria (1). Conversely, it will correct mydriasis caused by tonic pupil or third nerve palsy (2). In our patient’s case, pilocarpine administration did not result in pupillary constriction, supporting the diagnosis of drug-induced anisocoria.

Take-Home Points

  • Evaluation of acute anisocoria in the pediatric population can be challenging due to its wide range of potential etiologies including traumatic, neurologic, inflammatory, and pharmacologic causes. Though most commonly physiologic, anisocoria may represent a pediatric emergency due to the potential for underlying trauma or neurovascular compromise and thus a thorough neurologic exam and history is crucial (1, 20).

  • Inadvertent exposure to drugs such as glycopyrronium, a topical antiperspirant with anticholinergic properties, has been implicated in the pathogenesis of anisocoria in both adult and pediatric patients via inhibition of acetylcholine at the pupillary sphincter muscle (3-13). Other documented pharmacological causes of anisocoria include nebulized ipratropium bromide and scopolamine (14-19).

  • EM Clinicians should consider exposure-related anisocoria in the differential diagnosis of infant patients with acutely asymmetric pupils. In the absence of concerning neurologic findings, identification of potential drug exposures may help to minimize unnecessary testing and radiation exposure, sparing certain patients from time-intensive and costly interventions.

  • 1. Falardeau J. Anisocoria. Int Ophthalmol Clin. 2019;59(3):125-39.

  • 2. Payne WN, Blair K, Barrett MJ. Anisocoria. StatPearls. Treasure Island (FL): StatPearls Publishing Copyright © 2023, StatPearls Publishing LLC.; 2023.

  • 3. Pecha JD, Yen KG, Moisiuc A, et al. Anisocoria secondary to antiperspirant wipes in a pediatric population: a case series. J aapos. 2022;26(1):42-3.

  • 4. Chabicovsky M, Winkler S, Soeberdt M, et al. Pharmacology, toxicology and clinical safety of glycopyrrolate. Toxicol Appl Pharmacol. 2019;370:154-69.

  • 5. Coleman MJ, Tomsak RL. A 15-year-old girl with variable anisocoria. Digit J Ophthalmol. 2014;20(1):13-4.

  • 6. Micieli R, Micieli JA. Dilated Pupil in a Patient With Hyperhidrosis. JAMA. 2019;322(3):264-5.

  • 7. Radotra A, Baneke A, Paul B. Mydriasis secondary to use of glycopyrrolate cream. Br J Hosp Med (Lond). 2019;80(12):736.

  • 8. Pashaei-Marandi A, Assam JH, Arnold A, et al. Reversible anisocoria due to inadvertent ocular exposure to topical anticholinergic treatment for primary axillary hyperhidrosis. Can J Ophthalmol. 2019;54(6):e300-e2.

  • 9. Siscos SM, Figenshau K, Rajpara A. Use of gloves when applying topical glycopyrronium for treatment of primary axillary hyperhidrosis. J Am Acad Dermatol. 2020;83(4):e275.

  • 10. Kaufman AR, Gulati S, Curnyn KM. Pharmacologic anisocoria secondary to topical glycopyrronium for axillary hyperhidrosis: an emerging clinical presentation. Can J Ophthalmol. 2020;55(5):464.

  • 11. Al-Holou SN, Lipsky SN, Wasserman BN. Don’t Sweat the Blown Pupil: Anisocoria in Patients Using Qbrexza. Ophthalmology. 2020;127(10):1381.

  • 12. Kaufman AR, Gulati S, Pula JH, et al. Pharmacologic Mydriasis Secondary to Topical Glycopyrronium Tosylate Cloths: Clinical Characterization From a Multicenter Analysis. J Neuroophthalmol. 2022;42(4):530-4.

  • 13. Sandhu M, Eisenstein K. Mydriasis and anisocoria in a pediatric hyperhidrosis patient with interesting findings in the family cat. Pediatr Dermatol. 2023;40(1):210-1.

  • 14. Derinoz-Guleryuz O, Fidanci İ, Men-Atmaca Y. Nebulized Ipratropium Bromide-induced Anisocoria: Why Is Anisocoria Observed?. Iran J Allergy Asthma Immunol. 2021;20(1):125-128.

  • 15. Kokulu K, Öner H, Özen C, Eroğlu SE, Altunok İ, Akça HŞ. Pharmacologic anisocoria due to nebulized ipratropium bromide: A diagnostic challenge. Am J Emerg Med. 2019;37(6):1217.e3-1217.e4.

  • 16. Pejic R, Klaric B. Transient anisocoria in a patient treated with nebulized ipratropium bromide. Am J Ophthalmol Case Rep. 2017;7:11-13. Published 2017 Apr 12.

  • 17. Thiele EA, Riviello JJ. Scopolamine patchinduced unilateral mydriasis. Pediatrics. 1995;96(3 Pt 1):525.

  • 18. Rodor F, Cottin C, Jouglard J. Transdermal scopolamine and mydriasis. Therapie. 1989;44(6):447-448.

  • 19. Rubin MM, Sadoff RS, Cozzi GM. Unilateral mydriasis caused by transdermal scopolamine. Oral Surg Oral Med Oral Pathol. 1990;70(5):569-570.

  • 20. Gross JR, McClelland CM, Lee MS. An approach to anisocoria. Curr Opin Ophthalmol. 2016;27(6):486-492.

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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 |2025-01-04T22:33:55-08:00Jan 10, 2025|Ophthalmology, Pediatrics, SAEM Clinical Images|
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SAEM Clinical Images Series: Xylazine Wounds

A 32 year-old male with PMH significant for opioid use disorder, a prior admission in 2021 for left-sided empyema s/p thoracotomy and decortication, gas bacteremia, and tricuspid endocarditis presented for a left leg wound. The patient reported a wound to his left leg that had become larger over the past 5 months. The pain worsened today, prompting him to come to the emergency department for evaluation. His mother, who was at his bedside, reported that the same type of wound occurred on his right arm “many months ago” and resulted in his arm “falling off”. He injects heroin into his leg and denies licking his needles. He reported intermittent subjective fevers for the few days prior to presentation. He last used heroin 2 hours prior to arrival.

 

wounds

General: Patient appears very pale, cachectic, chronically ill.

HEENT: Mucus membranes dry.

Extremity: Right arm with exposed bone, wet gangrene noted to stump. Left calf with large wound, exposed muscle, and tendon noted. Movement of numerous maggots also noted throughout wound site. Patient unable to move leg secondary to pain.

CBC: Hgb 2.74 (compared to baseline of 9.0); WBC count 17.39

BMP: Na 126; K+ 5.9; Cr 2.7 (up from 0.69)

ESR: >100

CRP: 15.94

Necrotizing fasciitis

No, xylazine is a non-narcotic drug and is not an opioid, thus, Narcan will not specifically reverse acute xylazine intoxication. However, fentanyl is the most common drug combined with xylazine. Thus, Narcan is reasonable to administer in the setting of a suspected overdose since the patient’s presentation can be due to combined use.

Xylazine, commonly known as “tranq”, is causing an emerging public health concern that is not only associated with severe respiratory and central nervous system depression but as illustrated by this case, is infamous for disfiguring and life-threatening skin ulcers. Xylazine is a non-narcotic drug mainly utilized for sedation, pain relief, and muscle relaxation in veterinary medicine. In more recent human use, it can be injected into muscles and veins, insufflated, ingested, or smoked. It has a large volume of distribution due to its lipophilicity and is rapidly concentrated in the CNS and kidney, with an elimination half-life of approximately 23-50 minutes.

In regard to treating resulting wounds, antibiotic coverage for secondary infection of xylazine wounds must cover MRSA and coverage for group A streptococci should also be considered.

For managing xylazine withdrawal symptoms, the Philadelphia Department of Public Health’s most recent recommendations include replacement therapy with alpha-2-adrenergic agonists such as clonidine, dexmedetomidine, tizanidine, or guanfacine paired with symptom management for pain using short-acting opioids, ketamine, gabapentin, ketorolac, acetaminophen, or NSAIDs.

Take-Home Points

  • When treating xylazine wounds, assess for potential secondary infection including necrotizing fasciitis.

  • Use medications such as clonidine (alpha 2 receptor agonists) to manage symptoms of withdrawal, along with symptom management agents like short-acting opioids, ketamine, and NSAIDs.

  • Papudesi, Bhavani Nagendra, et al. Xylazine Toxicity – Statpearls – NCBI Bookshelf, www.ncbi.nlm.nih.gov/books/NBK594271/. Accessed 14 Dec. 2023.

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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 |2025-01-04T22:25:04-08:00Jan 6, 2025|SAEM Clinical Images, Tox & Medications|
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SAEM Clinical Images Series: Not Your Average Eczema

eczema

A 3-year-old male with a history of severe atopic dermatitis presented for facial rash and hand pain. Mom had been applying Aquaphor and Vaseline several times a day. On the day of presentation, he woke up with a new rash over his face and hands which prompted the ED visit. He is up to date on childhood immunizations and is not prescribed any oral medications.

 

Vitals: BP 103/61; HR 156; Temp 102.9°F; RR 30; SpO2 99%.

General: He appears in no acute distress, acting appropriately for age. Interacts and follows commands. Scratching himself all over.

Skin: Diffuse, itchy, dry skin throughout and findings noted in the attached images most notably erythematous pustules on the dorsal hands and peri-oral lesions in addition to punched-out ulcerations on the philtrum. Lesions are tender to palpation and spare mucous membranes and palms/soles. Nikolsky sign negative.

WBC: 12.96

Skin scraping: +VZV

This patient has Eczema herpeticum as demonstrated by multiple grouped pustules on an erythematous base.

Ophthalmology should be consulted to rule out ocular involvement most notably herpes zoster ophthalmicus.

Take-Home Points

  • Eczema herpeticum is typically caused by superinfection of Herpes Simplex Virus due to a diminished skin barrier from atopic dermatitis. It is commonly misdiagnosed as impetigo. Grouped vesicles/pustules on an erythematous base and tenderness to palpation should prompt the physician to suspect herpetic skin infection.
  • Eczema herpeticum may be potentially life-threatening if it has spread to multi-system involvement such as HSV keratitis or encephalitis.
  • Treatment includes acyclovir in addition to gram positive coverage such as TMP/SMX or cephalexin.

  • American Academy of Pediatrics: Herpes simplex. In: Kimberlin DW, Brady MT, Jackson MA, Long SS, eds. Red Book: 2015 Report of the Committee on Infectious Diseases. 30th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2015:432–445.
  • Studdiford JS, Valko GP, Belin LJ, Stonehouse AR. Eczema herpeticum: making the diagnosis in the emergency department. J Emerg Med. 2011 Feb;40(2):167-9. doi: 10.1016/j.jemermed.2007.11.049. Epub 2008 Jun 27. PMID: 18584994.

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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 |2024-12-02T22:01:54-08:00Dec 20, 2024|Dermatology, SAEM Clinical Images|
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SAEM Clinical Images Series: Pediatric Forehead Swelling

puffy

A 12-year-old male with a history of autism spectrum disorder and chronic sinusitis presented for forehead swelling. His mother reported that she noticed progressive forehead swelling for about one month. She had followed up with the patient’s pediatrician and ENT and was given oral cephalexin and fluticasone nasal spray which did not make any changes in his symptoms. The patient denied any fevers or headaches.

Vitals: Temp 97.4°F; BP 100/58; HR 90; RR 18; SpO2 98%.

General: Patient is comfortable appearing, in no acute distress.

ENT: 3×3 cm area of fluctuance centrally located over the forehead with no drainage or surrounding erythema that is minimally tender to palpation. No nasal drainage.

Neuro: Intact with no deficits.

WBC: 14.35

ESR: 23 mm/h

CRP: 0.74 mg/dL

CT demonstrates osteomyelitis of the frontal bone with osseous destruction with a 5 cm bifrontal complex loculated anterior epidural abscess as well as a 3 cm midline frontal subgaleal extracranial scalp abscess.

Findings are consistent with Pott’s Puffy Tumor.

Take-Home Points

  • Pott’s puffy tumor is a rare, life-threatening complication of frontal sinusitis characterized by osteomyelitis of the frontal bone with associated subperiosteal abscess causing swelling and edema over the forehead and scalp. It can be found in all age groups but is most common in adolescents.
  • MRI brain with and without contrast is the preferred imaging modality due to increased sensitivity to detect early intracranial and osseous abnormalities.
  • Treatment is typically surgical intervention with at least 6 weeks of intravenous antibiotics. The infection is typically polymicrobial warranting gram-positive, gram-negative, and anaerobic antibiotic coverage.

  • Sharma P, Sharma S, Gupta N, Kochar P, Kumar Y. Pott puffy tumor. Proc (Bayl Univ Med Cent). 2017 Apr;30(2):179-181. doi: 10.1080/08998280.2017.11929575. PMID: 28405074; PMCID: PMC5349820.
  • Masterson L, Leong P. Pott’s puffy tumour: a forgotten complication of frontal sinus disease. Oral Maxillofac Surg. 2009 Jun;13(2):115-7. doi: 10.1007/s10006-009-0155-7. PMID: 19352731.

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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 |2024-12-02T21:56:12-08:00Dec 16, 2024|Healthy in EM, HEENT, Infectious Disease, Pediatrics, SAEM Clinical Images|
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SAEM Clinical Images Series: My Mom Could Not See

retinal

An 87-year-old female with a history of hypertension, hyperlipidemia, chronic kidney disease stage IIIB, type 2 diabetes mellitus, and schizophrenia presented for evaluation due to sudden visual loss in her right eye, which began 12 hours before she arrived at the emergency department. She has experienced a sudden loss of vision in her right eye for more than six hours. She reports no eye pain or redness, nor has she experienced any flashing lights. Additionally, there have been no symptoms of numbness, tingling, headache, double vision, facial droop, slurred speech, temporal tenderness, jaw claudication, or localized weakness/numbness. Over the past one to two months, the patient has lost 30 pounds and has noted increasing weakness over the last several weeks.

 

Vitals: BP 136/46; Temp 97.2°F; HR 54; RR 16; SpO2 96% RA

Constitutional: Alert but doses off frequently, no acute distress, appeared weak.

Neuro: No facial droop, no tongue deviation, no dysarthria, strength 4+/5 throughout, normal finger to nose

HEENT: Normocephalic/atraumatic. No mass palpable. Conjunctiva normal on both eyes. EOMI. Decreased right eye light flex compared to the left eye, visual acuity on the left side can count fingers on the right side only seeing a light. No orbital swelling. Normal ear canal bilaterally, normal TM both sides. Septum midline. Oropharynx is clear and moist and mucous membranes are normal. No lymphadenopathy, no bruit.

CV: Regular rate and rhythm with normal S1 and S2, no murmurs.

MSK: Moves all extremities, no deformity, normal muscle tone.

Skin: Warm and dry. No skin rash.

CBC: WBC 9

Hgb: 8.8

Hct: 29.5

Plt: 394

CMP: Na 137, K 4.7, Cl 101, CO2 25, BUN 25, Cr 1.56

PT: 14.2

INR: 1.1

The fundoscopy of the right eye reveals a Central Retinal Artery Occlusion (CRAO), characterized by a pale retina with a cherry-red macula and “box-carring” of the blood vessels.

The potential causes of CRAO in elderly patients include Giant Cell Arteritis (GCA), atherosclerosis, or embolism. It is advisable to measure inflammatory markers, such as the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), particularly in patients over the age of 50. Despite the absence of temporal tenderness and jaw claudication, this patient’s non-specific systemic symptoms like weight loss and weakness, combined with elevated ESR (105) and CRP (6.8), heighten the suspicion of GCA as the etiology of the CRAO. Consultations with ophthalmology and rheumatology are warranted. Administering high-dose pulse steroids is crucial for preventing further complications, such as CRAO in the left eye. Additionally, evaluating non-arteritic causes of CRAO, including carotid artery imaging and echocardiography, should also be considered.

Take-Home Points

  • With acute painless vision loss, fundoscopy can aid in determining the differential diagnosis and further workup.
  • In CRAO, remember arteritic and non-arteritic causes.
  • Age cut off in CRAO will help to guide further work up.

  • Diagnosis and management of Central Retina Artery Occlusion. (2017). American Academy of Ophtalmology Eyenet magazine. [Online] Available at: https://www.aao.org/eyenet/ article/diagnosis-and-management-of-crao [Accessed 22 Dec 2023]
  • Guluma K, Lee JE. Ophtalmology. Rosen’s Emergency Medicine: Concepts and Clinical Practice 10th-ed. Edited by Ron Walls. Elsevier. 2023. 57, 750-780.e4

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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 |2024-12-02T21:51:58-08:00Dec 13, 2024|Ophthalmology, SAEM Clinical Images|
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SAEM Clinical Images Series: An On-Target Diagnosis

erythema

A 25-year-old female with no pertinent past medical history presented to an emergency department in Massachusetts with four days of generalized malaise, myalgias, congestion, low-grade fever, and a rash behind her left knee. The patient denied cough, shortness of breath, chest pain, abdominal pain, nausea, vomiting, and diarrhea. She lives with three roommates, none of whom were sick, and she denied any other known sick contacts. She also denied any occupational exposures or recent travel, although did endorse some recent hiking in the area.

Vitals: BP 128/84; HR 88; Temp 98°F; RR 18; SpO2 (on RA) 100%

General: Well appearing

HEENT: No conjunctival injection

Cardiovascular: S1, S2; no murmurs, rubs, or gallops

Skin: Erythematous patch with central clearing in left popliteal fossa

WBC: 5.1

Hgb: 12.6

Platelets: 223

Sodium: 139

Creatinine: 0.8

ALT/AST: 22/22

COVID/Influenza/RSV: negative

This clinical image depicts erythema migrans (EM), the classic rash seen in 70- 80% of early localized Lyme disease infections. Lyme disease is a bacterial infection caused by the spirochete Borrelia burgdorferi, transmitted through bites from Ixodes scapularis (Blacklegged Tick). Lyme disease is endemic to the northeastern part of the United States but is also commonly reported in the upper Midwest region of the country. There are three stages of Lyme disease: early localized infection, early disseminated infection, and late disseminated infection. Early localized infection starts 3-30 days after a tick bite. This stage is characterized by the EM rash as well as fatigue, low-grade fevers, malaise, myalgias, and lymphadenopathy. EM develops at the site of the tick bite, although only 25% of patients with the characteristic rash recall being bitten by a tick. Over the next several days, the rash will expand and may develop a central clearing. Thus, the rash is often described as appearing like a “bull’s eye” or a “target.” Serological testing may be negative in early Lyme disease thus diagnosis at this stage is usually clinical.

Treatment for early localized infection is typically Doxycycline 100mg PO BID x 10-14 days. Cefuroxime 500mg PO BID x 14 days is another option. Amoxicillin 500mg PO TID x 14 days is the preferred antimicrobial in patients who are pregnant and/or breast-feeding. As when treating infections caused by other spirochetes such as Treponema pallidum, a Jarisch- Herxheimer reaction may occur. Left untreated, disseminated disease will develop in 60% of patients. Most symptoms will occur within days to months, although late disseminated disease may take months to years to present. A wide range of clinical presentations are possible with early disseminated disease including diffuse annular skin lesions, meningoencephalitis, cranial nerve palsies (most commonly Bell’s Palsy), peripheral neuropathies, and AV nodal blocks. Late disseminated infection can present with transient, migratory oligoarticular arthritis and non-focal nervous system symptoms such as mild encephalopathy and fatigue. Serological studies in disseminated disease are highly sensitive and the CDC recommends two-step testing such as an enzyme immunoassay or immunofluorescent antibody assay followed by a Western blot if the initial testing is positive or equivocal. Treatment of disseminated Lyme depends on the systems involved. Given the ambiguity of early serologic testing and the potential for development of disseminated disease, erythema migrans is a clinical “can’t miss” dermatologic diagnosis in the emergency department.

Take-Home Points

  • Lyme disease is caused by bites from the Blacklegged Tick and is endemic to the northeastern United States.
  • Early localized Lyme infection often presents with the erythema migrans rash, a large targetoid or bull’s eye area of erythema with central clearing at the site of the tick bite.
  • The diagnosis of early Lyme is usually clinical and the three first-line antibiotics are Doxycycline, Cefuroxime, or Amoxicillin.

  • Kowalski TJ, Tata S, Berth W, Mathiason MA, Agger WA. Antibiotic treatment duration and long-term outcomes of patients with early lyme disease from a lyme disease- hyperendemic area. Clin Infect Dis. 2010 Feb 15;50(4):512-20. doi: 10.1086/649920. PMID: 20070237.
  • Lyme Disease. Centers for Disease Control and Prevention. 2022, Jan 19. https:// www.cdc.gov/lyme/
  • Steere AC. Lyme disease. N Engl J Med. 2001;345(2):115-125. doi:10.1056/NEJM200107123450207 4. Torbahn G, Hofmann H, Rücker G, Bischoff K, Freitag MH, Dersch R, Fingerle V, Motschall E, Meerpohl JJ, Schmucker C. Efficacy and Safety of Antibiotic Therapy in Early Cutaneous Lyme Borreliosis: A Network Meta-analysis. JAMA Dermatol. 2018 Nov 1;154(11):1292-1303. doi: 10.1001/jamadermatol.2018.3186. PMID: 30285069; PMCID: PMC6248135.

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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 |2024-12-02T21:38:35-08:00Dec 9, 2024|Dermatology, Infectious Disease, SAEM Clinical Images|
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