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

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

By |2026-02-19T12:56:37-08:00Feb 27, 2026|Uncategorized|

SAEM Clinical Images Series: Modern Pirate

ecchymosis

The patient is a 72-year-old male with multiple medical problems who presents to the Emergency Department complaining of dyspnea on exertion. The patient also complains of bruising that has developed on his right leg. He states that he previously had a similar episode for which she was admitted to the hospital and had warfarin discontinued due to thrombocytopenia. He also reports that he has been unable to eat or drink much lately due to gum swelling and tenderness, and states that when he begins chewing he feels as though his teeth are going to fall out. When asked about his usual diet, the patient states that he primarily eats raisin bran crunch and grits and that he does not really eat fruits or vegetables. He denies any chest pain, abdominal pain, nausea, vomiting, diarrhea, bloody stools, or any other complaints.

Vitals: All vital signs are normal.
General: Pleasantly interactive in no acute distress.
HEENT: Key findings are shown in the image provided.
Respiratory: Clear to auscultation, no increased work of breathing.
Extremities/Skin: Diffuse ecchymosis and petechiae are present. Bruising to the right foot and ankle as shown. Bilateral legs with significant petechiae diffusely. Hair as shown.

CBC: WBC 10.4 Hgb 7.8 Plt 98,000

RBC Morphology abnormal- Moderate Anisocytosis, Slight Poikilocytes
Moderate Polychromasia, Slight Elliptocytes, Slight Hyopchromia

CMP: Albumin 2.5, Total Protein 5.4

Scurvy results in multiple symptoms including gingivitis with bleeding, periodontal disease, loss of dentition, mucocutaneous petechiae, ecchymosis, hyperkeratosis, and corkscrew hairs. Scurvy is due to Vitamin C deficiency and resultant impaired collagen biosynthesis. Petechiae, ecchymosis, follicular hyperkeratosis, perifollicular hemorrhages, corkscrew hairs, gingival bleeding, arthralgias, skin discoloration, impaired wound healing, koilonychias, and splinter hemorrhages may all be seen in patients with scurvy. These findings are primarily derived from inability to synthesize collagen due to lack of ascorbic acid, which is used as an electron donor to catalyze proline and lysine into hydroxyproline and hydroxylysine. Ascorbic acid also prevents epigenetic DNA hypermethylation, which is essential in the synthesis of certain collagen types.

Take-Home Points

  • A thorough dietary history can help identify patients at risk for vitamin deficiencies and other diagnoses caused by malnutrition.
  • Scurvy is caused by Vitamin C deficiency and results in impaired collagen synthesis, leading to multiple potential abnormal physical exam findings such as gingivitis with bleeding, severe periodontal disease, loss of dentition, mucocutaneous petechiae, ecchymosis, hyperkeratosis, and corkscrew hairs.

  • Gandhi M, Elfeky O, Ertugrul H, Chela HK, Daglilar E. Scurvy: Rediscovering a Forgotten Disease. Diseases. 2023 May 26;11(2):78. doi: 10.3390/diseases11020078. PMID: 37366866; PMCID: PMC10296835.
  • Léger D. Scurvy: reemergence of nutritional deficiencies. Can Fam Physician. 2008 Oct;54(10):1403-6. PMID: 18854467; PMCID: PMC2567249.

By |2026-02-19T12:33:13-08:00Feb 23, 2026|SAEM Clinical Images, Uncategorized|

SAEM Clinical Images Series: A Mucous Membrane Mystery

eye

The patient is a healthy 14-year-old male without past medical history who presents to the Emergency Department with oral lesions, eye swelling, intermittent fevers, and pain with urination. Over the past 10 days he has been seen by his PCP and at an outside ED for a cough, sore throat, fevers, and oral pain. Three days ago he was seen by his PCP, had a positive rapid strep test, and was started on amoxicillin. His oral lesions and lip swelling have been progressively worsening over the past 2 days. Monospot testing was also performed yesterday and is negative. Today he was seen again by his PCP for new pain with urination and was sent to the ED for concern for Kawasaki disease. The patient has had decreased oral intact due to his pain, but otherwise has no other complaints.

Vitals: BP 124/88 HR 112 R 28 T 100.2 F O2sat 94% room air.
HEENT: Relevant findings are shown in the images provided. Tonsillar exudate is present. No meningismus. Voice is normal.
Respiratory: Coarse breath sounds with diffuse wheezing.
Cardiovascular: Tachycardic, no murmurs, no rubs.
Skin: No rash. Negative Nikolsky sign. No palmar desquamation.
Lymph: Cervical lymphadenopathy is present
Genitourinary: See image provided.

CBC, CMP, Urinalysis: negative

COVID/Flu/RSV: negative

Mycoplasma NAAT: positive.

CRP: 13.5 mg/L

ESR: 48 mm/Hr

This child has RIME (reactive infections mucocutaneous eruption), a rare post-infectious cause of mucositis in children and adolescents.

Prolonged fevers and illnesses are frequent reasons for pediatric ED visits. Children and adolescents can be more prone than adults to a variety of immune-mediated and other inflammatory reactions such as Kawasaki disease, serum sickness like reactions, erythema or urticaria multiforme, SJS/TEN, MISC, among others. RIME is a relatively recently described post-infectious condition characterized by mucositis in at least two mucus membranes, with or without an area of cutaneous eruption. It was previously called mycoplasma-induced rash and mucositis (MIRM), and mycoplasma is the most common trigger, though the designation RIME implies that other common infectious agents (covid, influenza, and other viral and bacterial pathogens) have been identified as causal agents. Management is supportive, including treatment of the underlying illness (in this case, treatment of mycoplasma). Corticosteroids and other immunomodulatory agents may be used in more severe cases.

Take-Home Points

  • RIME is a reaction primarily involving mucosal surfaces that is often associated with Mycoplasma pneumoniae infections in pediatric populations.
  • Treatment of RIME involves treating Mycoplasma pneumoniae with azithromycin and supportive care including hydration and appropriate consultations for wound management as needed.

  • Lofgren D, Lenkeit C. Mycoplasma Pneumoniae-Induced Rash and Mucositis: A Systematic Review of the Literature. Spartan Med Res J. 2021 Aug 30;6(2):25284. doi: 10.51894/001c.25284. PMID: 34532621; PMCID: PMC8405277.
  • Meyer Sauteur PM, Theiler M, Buettcher M, Seiler M, Weibel L, Berger C. Frequency and Clinical Presentation of Mucocutaneous Disease Due to Mycoplasma pneumoniae Infection in Children With Community-Acquired Pneumonia. JAMA Dermatol. 2020 Feb 1;156(2):144-150. doi: 10.1001/jamadermatol.2019.3602. PMID: 31851288; PMCID: PMC6990853.
  • Rehmus, W. E., Phillips, J., & Flegel, L. (2023). In Pediatric Dermatology (pp. 274–274). essay, UBC LIBRARY. Retrieved January 6, 2025,.

By |2026-02-06T12:12:18-08:00Feb 20, 2026|SAEM Clinical Images, Uncategorized|

SAEM Clinical Images Series: An Expanding Painful Neck Mass

Mass

The patient is a 20-year-old male who presents to the Emergency Department complaining of painful and rapidly worsening swelling in the anterior neck over the last three days. The patient reports that he had a similar episode in the past for which he was prescribed antibiotics and underwent a needle aspiration procedure at the base of his mouth, which led to resolution of his symptoms. The patient reports subjective chills, change in voice, sore throat, and painful swallowing. He is able to tolerate oral secretions and denies difficulty breathing. He has no other complaints at this time. A bedside ultrasound exam and CT of the patient’s neck were subsequently performed.

Vitals: BP 147/69, HR 68, RR 18, Temp 100.6, SpO2 98% room air.
General: Nontoxic but in obvious discomfort. Able to tolerate brief
periods in a supine position. Speaking with mild stridor.
HEENT:
Neck as shown. Swollen area is warm with no induration or
crepitus. Neck supple. No mastoid tenderness, normal appearing tympanic
membranes. No trismus. Normal dentition.
Respiratory:
Mild biphasic stridor but normal work of breathing.
Cardiovascular:
Regular rate and rhythm, no murmur.

WBC 18.0
Rapid Group A Strep swab: negative.
Monospot screen: negative
HIV antibody/antigen: negative.

Deep space infection of the neck, Ludwig’s Angina.

The patient has a plunging ranula.

Deep space infections of the neck can be categorized by the fascial layer involved: superficial, middle, and/or deep. Infections in the deep- superficial and deep-middle fascia include Ludwig’s angina, mandibular abscesses, and parotitis. These are most often caused by dental infections, and can cause compression resulting in airway compromise, thrombophlebitis, and narrowing of the great vessels of the neck. Infection of the deep layer of the cervical fascia, such as in retropharyngeal or parapharyngeal abscess, communicates directly with the mediastinum, and can rapidly progress to severe mediastinitis. This patient’s imaging shows cystic structures with no flow seen within or around the structures, and shows the fluid collection extending from the sublingual space, communicating with the submandibular space and base of the mouth. This was determined to be an infected plunging ranula.

Take-Home Points

  • A simple ranula (occurs in 1 out of 5000 individuals) presents as a painless bluish saliva containing cyst visualized below the tongue.
  • A “plunging” (or “diving”) ranula is a rare condition caused by direct leakage of salivary fluid from the sublingual gland at the base of the mouth into the soft tissues of the neck.
  • Treatment involves needle aspiration and surgical excision. About 50% of cases recur without excision of the submandibular gland.

  • Almuqamam M, Gonzalez FJ, Sharma S, et al. Deep Neck Infections. [Updated 2024 Aug 11]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.
  • Kalra V, Mirza K, Malhotra A. Plunging ranula. J Radiol Case Rep. 2011;5(6):18-24. doi: 10.3941/jrcr.v5i6.682. Epub 2011 Jun 1. PMID: 22470797; PMCID: PMC3303342.
  • Olojede ACO, Ogundana OM, Emeka CI, et al. Plunging ranula: surgical management of case series and the literature review. Clin Case Rep. 2017;6(1):109-114. Published 2017 Nov 29. doi:10.1002/ccr3.1272

By |2026-01-06T10:03:30-08:00Jan 7, 2026|Uncategorized|

SAEM Clinical Images Series: Tongue Twisters

tongue
The patient is a 68-year-old male with a past medical history of hypertension who presents to the Emergency Department for evaluation of tongue swelling. The patient reports that his left tongue was swollen 3 weeks ago. He was evaluated, prescribed Levaquin, and was advised to gargle peroxide/salt water per his primary care provider. The swelling resolved after approximately 2 days. This morning, he awoke at 2 AM with swelling in the right side of his tongue. He denies any allergies or prior intubations. He denies any new foods, exposures, any other complaints at this time. He states that his tongue has not increased in size since awakening. The patient has been on no new medications and has taken enalapril daily for the past 10 years.

Vitals: BP 130/90, HR 77, RR 14, T 97.8F, O2sat 99% room air.

General: Comfortable, no signs of distress, voice tone is clear but he has difficulty articulating his words due to his tongue swelling.
HEENT: Relevant findings are shown in the image provided. Uvula midline. Mallampati class 2 airway.
Neck: Supple, no stridor.
Cardiovascular: Regular rate, rhythm, normal peripheral pulses.
Skin: No rash or urticaria seen.

ACE-inhibitor-induced angioedema.

Our patient presented to the ED complaining of unilateral tongue swelling in the setting of enalapril as his only medication, making ACE-inhibitor- induced angioedema his most likely diagnosis. ACE-inhibitor-induced angioedema can occur at any point during the course of treatment (our patient had been on enalapril for ten years). Non-histaminergic (non- allergic) angioedema is typically a result of elevated bradykinin levels. Classification of angioedema includes four subtypes: Hereditary angioedema with or without C1 esterase inhibitor deficiency, acquired C1 esterase inhibitor deficiency, ACE-inhibitor-induced angioedema, and idiopathic angioedema. ACE-inhibitor induced angioedema has an overall incidence of 0.3% to 0.7% and is 3 to 4 times more likely in African-Americans. Females are at a 50% higher risk than males. Airway compromise is the most feared complication of angioedema. In cases requiring intubation, advanced airway setups and techniques along with surgical backup is advisable.

Take Home Points

1. ACE-inhibitor-induced angioedema does not respond to epinephrine and treatment is mainly supportive.
2. In severe cases requiring intubation, awake fiberoptic intubation is a preferred method when accessible and feasible, and paralytics should be utilized with caution.

  1. Frank MM, Gelfand JA, Atkinson JP. Hereditary angioedema: the clinical syndrome and its management. Ann Intern Med. 1976;84:580–593. doi: 10.7326/0003-4819-84-5-580.
  2. Lee JH, Cho JY, Nam DH, Hong CS. A case of hereditary angioedema. Allergy. 1994;14:695–701. Weis M. Clinical review of hereditary angioedema: diagnosis and management. Postgrad Med. 2009;121:113–120. doi: 10.3810/pgm.2009.11.2071.

By |2025-10-27T08:32:23-07:00Oct 20, 2025|ENT, SAEM Clinical Images, Uncategorized|
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